Growth factor pre-treatment differentially regulates phosphoinositide turnover downstream of lysophospholipid receptor and metabotropic glutamate receptors in cultured rat cerebrocortical astrocytes

Reactive gliosis is an aspect of neural plasticity and growth factor (GF) stimulation of astrocytes in vitro is widely regarded as a model system to study astrocyte plasticity. Astrocytes express receptors for several ligands including lysophosphatidic acid (LPA) and sphingosine-1-phosphate (S1P), agonists for the G-protein-coupled lysophospholipid receptors (lpRs). Activation of lpRs by LPA or S1P leads to multiple pharmacological effects including the influx of calcium, phosphoinositide (PI) hydrolysis, phosphorylation of extracellular receptor regulated kinase (ERK), release of arachidonic acid, and induces mitogenesis. Treatment of astrocytes in vitro with a growth factor cocktail (containing epidermal growth factor [EGF], basic fibroblast growth factor [bFGF] and insulin) led to a marked attenuation of lpR-induced PI hydrolysis. In contrast, under identical conditions, GF treatment led to marked potentiation of PI hydrolysis downstream of activation of another abundantly expressed G-protein coupled receptor, mGluR5. Quantitative gene expression analysis of GF-treated or control astrocytes by TaqMan RT-PCR indicated that GF treatment did not change gene expression of lpa1 and s1p1, but increased gene expression of s1p5 which is expressed at very low levels in basal conditions. These results suggest that GF differentially affected PLC activation downstream of mGluR5 versus lpR activation and that the changes in mRNA levels of lpRs do not account for marked attenuation of agonist-induced phosphoinositide turnover.     

Long-term effects of physiologic concentrations of dexamethasone on human bone-derived cells

Bone cells derived from human trabecular explants display osteoblastic features. We examined the modulation of alkaline phosphatase activity and cAMP production as the result of exposing trabecular explants to physiologic concentrations of dexamethasone for 4 weeks during cellular outgrowth and subculture. Cells treated with dexamethasone were observed to grow generally more slowly than control cells. Cells appeared larger and more polygonal, and staining for alkaline phosphatase was more intense in the dexamethasone-exposed cultures. There was a progressive increase in cellular PTH responsiveness with increasing duration of exposure of cells to dexamethasone. Cells grown for 6 weeks in 3 x 10(-8) M dexamethasone had a 10-fold increase in PTH-stimulated cyclic AMP accumulation. Dexamethasone-treated cells also had a significantly increased alkaline phosphatase activity. 1,25-(OH)2D3-stimulated alkaline phosphatase activity was increased approximately 20-fold. cAMP responses were significantly increased to PTH (21.7-fold), PGE1 (2.67-fold), and forskolin (4.81-fold), but not to cholera toxin. Dexamethasone-treated cells also had a mean decrease in 1,25-(OH)2D3-stimulated osteocalcin production to 26.2% of control values (p less than 0.001). Hydrocortisone treatment gave rise to similar effects but of smaller magnitude than those of dexamethasone. Testosterone did not have a significant effect on alkaline phosphatase activity or cAMP production. Skin fibroblasts showed a significant enhancement of alkaline phosphatase activity in response to dexamethasone, but of a much smaller magnitude than in bone cells. The phenotypic changes induced by long-term culture in dexamethasone are consistent with the promotion of a more differentiated osteoblastic phenotype.     

粉防己碱与牛磺酸合用对血小板聚集与血栓形成的影响

粉防己碱（Ｔｅｔ）和牛磺酸（Ｔａｕ）均能抑制ＡＤＰ、胶原和凝血酶诱导的大鼠血小板聚集及血栓形成。Ｔｅｔ抑制ＡＤＰ诱导聚集较强，Ｔａｕ则对胶原作用最明显，二药减半量合并应用时，较各药单用强     

大肝癌手术切除探讨（附16例分析）

报告16例大肝癌手术切除治疗效果，癌块直径>7cm。其中巨块型12例，癌块>10cm9例；癌块>14cm3例，均经病理证实。Ⅱ期切除3例，均经肝固有动脉结扎加插管注药化疗，肿块缩小后再手术，术后生存1年4例，2年3例，3年4例，4年1例，全组中位生存期24.1个月，并对大肝癌的手术适应证及术式选择等进行了探讨。     

Magnetic resonance imaging in full-term infants with repetitive focal seizures.

We report two full-term infants who developed repetitive focal seizures within the first 48 hours of life. Neither infant had predisposing factors and there were no abnormalities on a computed tomography (CT) scan performed on day 2 of life. Magnetic resonance imaging (MRI) performed during the second week of life showed a focal hemorrhagic infarction in both patients. We conclude that either an MRI or a contrast-enhanced CT scan should be obtained within 1 week in patients in whom the initial imaging technique failed to reveal a focal lesion, at which time a cerebral infarction can be diagnosed with greater sensitivity.     

Role of balloon angioplasty in the treatment of aortic coarctation.

Since the initial report of coarctation balloon angioplasty in 1982, several groups have used this technique for native coarctations in neonates, infants, and children and for postoperative recoarctations. However, recommendations for use of balloon angioplasty as a treatment procedure of choice are clouded by reports of aneurysm development at the site of coarctation. Here we review our experience as well as that published in the literature, including Valvuloplasty and Angioplasty of Congenital Anomalies Registry data, and present evidence in support of balloon angioplasty as a therapeutic procedure of choice for treating native and recurrent postoperative aortic coarctations. Balloon angioplasty of native aortic coarctations in 20 neonates and infants 1 year old or less reduced peak systolic pressure gradient across the coarctation from 40 +/- 12 mm Hg (mean +/- standard deviation) to 11 +/- 8 mm Hg (p less than 0.001); no patient required immediate surgical intervention. The residual gradient at follow-up (mean follow-up, 12 months) in 16 infants was 18 +/- 16 mm Hg, a significant improvement (p less than 0.01) compared with preangioplasty values. In none of the patients did an aneurysm develop. Recoarctation developed in 5 (31%) of the 16 infants and was successfully treated either by surgical resection (in 2) or by repeat balloon angioplasty (in 3). A comparison of mortality and recurrence rates between the balloon angioplasty and surgical groups was made with the help of data pooled from the literature published since 1980. The initial (7% versus 23%) and late (2% versus 25%) mortality and recoarctation (11% versus 18%) rates were higher (p less than 0.025) after surgical intervention than after balloon therapy. When only reports in which patients were operated on after 1979 were included in this type of analysis, the initial and late mortality rates remained higher (p less than 0.01) after operation than after angioplasty, and the recoarctation rates became similar (p greater than 0.1). Thirty-two children (greater than 1 year old) underwent balloon angioplasty of native coarctation with a resultant reduction in peak systolic pressure gradient from 48 +/- 19 mm Hg to 10 +/- 9 mm Hg (p less than 0.001), which continued to remain low (14 +/- 11 mm Hg; p less than 0.001) at follow-up catheterization in 24 children 13 months (mean) later. There were no immediate or late deaths. A small aneurysm developed in 1 patient (4%) but did not require intervention. Recoarctation developed in 2 patients (8%), and in both, repeat balloon angioplasty was performed with good results.(ABSTRACT TRUNCATED AT 400 WORDS)     

Postsurgical conjunctival epithelial cysts.

MR appearance of two patients with large, orbital conjunctival epithelium-lined inclusion cysts are presented. Both were complications of ophthalmic surgical procedures that necessitated conjunctival incision.     

仿冒进口白兰地酒类快速鉴别方法初探

本文通过对南海市查获的仿冒干邑白兰地的检验，发现其pH值、酒精度、甲醇、杂醇油含量与真品的差别具有统计学显著性意义；伪品的蒸馏残留物不同于真品；部分伪品的色泽来自无机染料，为我国食品卫生标准所禁用。     

Spatio-temporal expression of estrogen sulfotransferase within the hepatic lobule of male rats: implication of in situ estrogen inactivation in androgen action.

Estrogen sulfotransferase (EST) catalyzes transfer of the sulfate group from phosphoadenosine phosphosulfate to estrogenic steroids. Since estrogen sulfates do not bind to the estrogen receptor with high affinity, EST can control the intracellular level of the receptor-active estrogens. Androgen action in the rat liver, as indicated by the androgenic induction of alpha 2u-globulin, is inhibited by low levels of estrogens. Thus, in situ estrogen inactivation by EST is expected to increase hepatic androgen sensitivity. During the lifespan of the animal, rat liver undergoes three distinct phases of androgen sensitivity, i.e. prepubertal androgen insensitivity, androgen sensitivity after approximately 40 days of age, and androgen insensitivity during senescence (greater than 750 days). EST in the liver is expressed only after puberty, when the liver becomes androgen sensitive. Furthermore, localization of EST and its corresponding mRNA within the lobular unit of the liver demonstrates that only androgen-responsive hepatocytes located around the central vein contain immunoreactive EST and its corresponding mRNA. These temporal and spatial correlations of EST expression and hepatic androgen sensitivity support the concept that steroid-inactivating enzymes play important roles in sex hormone action.