L'intoxication alloxanique chez la femelle gravide de cobaye

Sommaire Chez la femelle de cobaye gravide, une injection intracardiaque de 200 mg/kg d'alloxane provoque en 6–8 hs, une pycnose généralisée des cellules B des îlots endocriniens du pancréas; 18–20 hs après l'injection, les acini exocrines en bordure des îlots devenus nécrotiques se différencient et prolifèrent des cordons de cellules endocriniennes. Cette régénération intense et rapide est pratiquement achevée 42 hs après l'injection.L'effet, sur le pancréas foetal, de l'alloxane injectée à la femelle gravide, varie suivant le stade de développement atteint par le tissu endocrine au moment de l'injection. Pendant la phase de différenciation, aux dépens de l'épithélium des canaux, des premières cellules A (emb. de 13 mm, 25e jour) et B (emb. de 27 mm, 34e jour), puis de prolifération de cordons aboutissant à la formation des îlots primitifs dits îlots à manteau (foetus de 58 mm, 43e jour), les cellules B sont totalement réfractaires à l'action de l'alloxane. Chez les foetus ayant atteint 75 mm (50–51e jour), les premiers îlots à architecture définitive ont fait leur apparition par remaniement secondaire des îlots à manteau, processus qui continuera jusqu'à la naissance. Dès que ce stade est atteint, l'alloxane injectée à la mère provoque la pycnose généralisée des cellules B dans les îlots définitifs alors que les îlots à manteau voisins restent intacts. Il semble donc que les cellules B doivent atteindre un certain degré de maturité pour être sensibles à l'alloxane.     

CYTOGENETIC STUDIES IN THE GENUS TRIBOLIUM (POACEAE: ARUNDINEAE)

The genus Tribolium Desv. consists of nine species, i.e., T. utriculosum (Nees) Renv., T. ciliare (Stapf) Renv., T. echinatum (Thunb.) Desv., T. hispidum (Thunb.) Desv., T. acutiflorum (Nees) Renv., T. obliterum sensu Davidse, T. glomeratum sensu Davidse, T. uniolae (L.f.) Renv., and T. brachystachyum (Nees) Renv. The genus has a basic chromosome number of 6, and from diploid to hexaploid specimens have been examined. Precocious segregation of metaphase I bivalents were observed in four species. Multivalent formation results in unequal chromosome segregation during anaphase I, and several cells with an 11–13 chromosome distribution have been observed. The presence of univalents and anaphase I bridges in all T. brachystachyum specimens suggests a hybrid origin for the species. B-chromosomes were present in specimens from four species. The B-chromosomes are similar to the euchromosomes with the exception that they do not participate in meiosis. The B-chromosomes have a possible isochromosome origin. The cytogenetic evidence presented supports the combination of Plagiochloa and Lasiochloa into Tribolium and indicates that the genus is closely related to Urochlaena, whereas it is not closely related to Prionanthium.     

Infectivity of preserved Cryptosporidium parvum oocysts for immunosuppressed adult mice

Abstract The present study was undertaken to determine the infectivity of Cryptosporidium parvum oocysts for immunosup-pressed adult C57BL/6N mice after the oocysts had been stored from 1–48 months at 4°C in 2.5% potassium dichromate. All mice inoculated with oocysts 1–18 months old developed patent infections, while mice inoculated with older oocysts remained uninfected. The prepatent period was extended from 2 to 6 or 7 days as the storage time for oocysts increased. The finding that C. parvum oocysts remain infective for mice for at least 18 months offers important economic and time-saving advantages for investigators who frequently require large numbers of oocysts that must be painstakingly purified from calf manure.     

肝炎平对D－氨基半乳精所致肝损害保护作用的酶组织化学研究

本实验采用Ｄ－氨基半乳糖（Ｄ－ＧａｌＮ）诱导的大鼠急性肝损伤模型,观察大鼠肝脏组织化学的变化,探讨肝炎平对急性肝损伤的保护作用。实验分为四组,即正常对照组、模型组、肝炎平及肝得健保护组。结果表明：肝炎平对肝细胞膜系统有一定的保护作用。肝炎平组和肝得健组ＳＤＨ、ＣＣＯ及ＣｈＥ活性明显高于模型组,且与正常对照组相近。本实验模型组ＡＣＰ的活性明显高于正常组,而肝炎平组ＡＣＰ的活性明显低于模型组,与正常对照组无显著性差异。提示：肝炎平可显著改善因Ｄ－氨基半乳糖所致肝损害的作用。且其对肝细胞的保护作用与肝得健一致。     

中药固真方对一些与细胞增殖有关基因表达的影响

 中药固真方对一些与细胞增殖有关基因表达的影响姚明忠,顾文聪,丁卫,韩志芬,杜国光（上海中医药大学生物化学教研室,上海２０００３２）（北京医科大学生物化学与分子生物学系,北京１０００８３）中药固真方（ＶＲＦ）具有补肾益精、延缓衰老的作用［１］．能提高成...     

Forskolin对成骨样细胞蛋白激酶C及三磷酸肌醇的影响

Ｆｏｒｓｋｏｌｉｎ（ＦＳＫ）是一种植物二萜类化合物,为腺苷酸环化酶的特异激活剂,实验发现：ＦＳＫ和作为参照的诱导分化剂维甲酸（ＲＡ）单独或联合应用均可升高胞浆蛋白激酶Ｃ（ＰＫＣ）活性,并降低膜ＰＫＣ活性,ＦＳＫ可使表皮生长因子（ＥＧＦ）诱导的细胞内三磷酸肌醇（ＩＰ３－１,４,５）水平降低至对照组的４４．４％至６７％;ＦＳＫ与ＲＡ合用可显著降低成骨样细胞特征蛋白碱性磷酸酶（ＡＫＰ）的活性。以上结果表明,ＦＳＫ对成骨样细胞内磷脂酰肌醇信息传递体系有深刻影响,可能与其调节细胞的增殖分化有关。     

大鼠不同脑区突触体钙水平的年龄差异

本实验使用荧光指示剂Ｆｕｒａ－２与Ｔｂ~（３＋）,检测了不同年龄组大鼠的不同脑区（海马、皮层、间脑、小脑）突触体内游离钙与膜结合钙水平。结果显示,与青年对照组相比,老年大鼠大部分脑区（海马、皮层、间脑）突触体内游离钙水平显著增高,尤其是海马突触体内游离钙增高极为显著;其突触体膜结合钙水平表现为：海马、小脑两脑区明显升高,而皮层、间脑两脑区明显下降,呈现一种全脑范围内的钙水平失衡。提示动物的衰老与其脑内钙自体平衡失调有关。     

The 3-D structure of a zinc metallo-beta-lactamase from Bacillus cereus reveals a new type of protein fold.

The 3-D structure of Bacillus cereus (569/H/9) beta-lactamase (EC 3.5.2.6), which catalyses the hydrolysis of nearly all beta-lactams, has been solved at 2.5 A resolution by the multiple isomorphous replacement method, with density modification and phase combination, from crystals of the native protein and of a specially designed mutant (T97C). The current model includes 212 of the 227 amino acid residues, the zinc ion and 10 water molecules. The protein is folded into a beta beta sandwich with helices on each external face. To our knowledge, this fold has never been observed. An approximate internal molecular symmetry is found, with a 2-fold axis passing roughly through the zinc ion and suggesting a possible gene duplication. The active site is located at one edge of the beta beta sandwich and near the N-terminal end of a helix. The zinc ion is coordinated by three histidine residues (86, 88 and 149) and a water molecule. A sequence comparison of the relevant metallo-beta-lactamases, based on this protein structure, highlights a few well-conserved amino acid residues. The structure shows that most of these residues are in the active site. Among these, aspartic acid 90 and histidine 210 participate in a proposed catalytic mechanism for beta-lactam hydrolysis.     

A role for cAMP in angiotensin II mediated inhibition of cell growth in AT1A receptor-transfected CHO-K1 cells

G-protein coupled Angiotensin II receptors (AT_1A), mediate cellular responses through multiple signal transduction pathways. In AT_1A receptor-transfected CHO-K1 cells (T3CHO/AT_1A), angiotensin II (AII) stimulated a dose-dependent (EC₅₀=3.3 nM) increase in cAMP accumulation, which was inhibited by the selective AT₁, nonpeptide receptor antagonist EXP3174. Activation of protein kinase C, or increasing intracellular Ca²⁺ with ATP, the calcium ionophore A23187 or ionomycin failed to stimulate cAMP accumulation. Thus, AII-induced cAMP accumulation was not secondary to activation of a protein kinase C- or Ca²⁺/calmodulin-dependent pathway. Since cAMP has an established role in cellular growth responses, we investigated the effect of the AII-mediated increase in cAMP on cell number and [³H]thymidine incorporation in T3CHOA/AT_1A cells. AII (1 M) significantly inhibited cell number (51% at 96 h) and [³H]thymidine incorporation (68% at 24 h) compared to vehicle controls. These effects were blocked by EXP3174, confirming that these responses were mediated through the AT₁ receptor. Forskolin (10 M) and the cAMP analog dibutyryl-cAMP (1 mM) also inhibited [³H]thymidine incorporation by 55 and 25% respectively. We extended our investigation on the effect of AII-stimulated increases in cAMP, to determine the role for established growth related signaling events, i.e., mitogen-activated protein kinase activity and tyrosine phosphorylation of cellular proteins. AII-stimulated mitogen-activated protein kinase activity and phosphorylation of the 42 and 44 kD forms. These events were unaffected by forskolin stimulated increases in cAMP, thus the AII-stimulated mitogen-activated protein kinase activity was independent of cAMP in these cells. AII also stimulated tyrosine phosphorylation of a number of cellular proteins in T3CHO/AT_1A cells, in particular a 127 kD protein. The phosphorylation of the 127 kD protein was transient, reaching a maximum at 1 min, and returning to basal levels within 10 min. The dephosphorylation of this protein was blocked by a selective inhibitor of cAMP dependent protein kinase A, H89-dihydrochloride and preexposure to forskolin prevented the AII-induced transient tyrosine phosphorylation of the 127 kD protein. These data suggest that cAMP, and therefore protein kinase A can contribute to AII-mediated growth inhibition by stimulating the dephosphorylation of substrates that are tyrosine phosphorylated in response to AII.