[Illustrations de Kalendarium] / [Non identifié] ; Johann Regiomontanus, aut. du texte

Comprend : [Pl. : calendrier d es éclipses de lune et de soleil de 1475 à 1479.] [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : calendrier d es éclipses de lune et de soleil de 1479 à 1482.] [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : calendrier d es éclipses de lune et de soleil de 1483 à 1487.] [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : calendrier d es éclipses de lune et de soleil de 1487 à 1491.] [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : calendrier d es éclipses de lune et de soleil de 1493 à 1497.] [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : calendrier d es éclipses de lune et de soleil de 1497 à 1504.] [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : calendrier d es éclipses de lune et de soleil de 1505 à 1513.] [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : calendrier d es éclipses de lune et de soleil de 1515 à 1518.] [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : calendrier d es éclipses de lune et de soleil de 1519 à 1523.] [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : calendrier d es éclipses de lune et de soleil de 1523 à 1530.] [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : cadran solaire.] Instrumentum Horarum inaequalium. [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : calendrier lunaire.] Instrumentum veri motus lunae minue. Adde. [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : cadran solaire.] Quadrans Horologii Horizontalis. [Cote : Res g V 57/Microfilm R 16374] ; [Pl. : cadran solaire.] Quadratum Horarium Generale. [Cote : Res g V 57/Microfilm R 16374]

Preimplantation genetic diagnosis (PGD) for HLA typing: bases for setting up an open international collaboration when PGD is not available.

In severe forms of Diamond-Blackfan anemia, preimplantation genetic diagnosis (PGD) of histocompatibility leukocyte antigen-compatible embryos for enabling the next sibling in the family to be a stem-cell transplantation donor constitutes the sole lasting cure capable of terminating the enduring need for iterative transfusions. We report here an open collaboration between two renowned institutions to provide a family desiring this treatment even though they resided where the preimplantation genetic diagnosis procedure is banned.

Estradiol levels in men with congenital hypogonadotropic hypogonadism and the effects of different modalities of hormonal treatment.

Objective: To evaluate the degree of E-2 deficiency in male congenital hypogonadotropic hypogonadism (CHH), and its response to different hormonal treatments.Design: Retrospective and prospective studies.Setting: Academic institution.Patient(s): Untreated or treated CHH, healthy men, untreated men with Klinefelter syndrome (KS). Intervention(s): Serum sex hormone-binding globulin (SHBG) and total E-2 (TE2) as well as bioavailable (BE2) and free (FE2) levels were measured and determined.Main Outcome Measure(s): Total, bioavailable, and free testosterone, TE2, BE2, FE2 were compared in normal men, untreated and treated CHH and in untreated KS.Result(s): TE2, BE2, and FE2 levels were very significantly lower in untreated patients with CHH (n = 91) than in controls (n = 63) and in patients with KS (n = 45). The TE2 correlated positively with serum total T in patients with CHH. The TE2 also correlated very positively with serum LH in the combined population of patients with CHH and healthy men, suggesting that low E-2 levels in CHH are due to severe LH-driven T deficiency. All fractions of circulating E-2 were very significantly higher in patients with CHH receiving T enanthate (n = 101) or the FSH-hCG combination (n = 88) than in untreated patients with CHH. Contrary to dihydrotestosterone (DHT), both T enanthate and combined FSH-hCGtherapy significantly and prospectively increased TE2 levels in patients with CHH.Conclusion(s): Contrary to KS, the male hypogonadism observed in CHH is associated with profound E-2 deficiency, which can be overcome by aromatizable androgen or combined gonadotropin therapy. (Fertil Steril (R) 2011; 95: 2324-29. (C) 2011 by American Society for Reproductive Medicine.)

Glucose uptake, utilization, and signaling in GLUT2-null islets.

We previously reported that pancreatic islet beta-cells from GLUT2-null mice lost the first phase but preserved the second phase of glucose-stimulated insulin secretion (GSIS). Furthermore, we showed that the remaining secretory activity required glucose uptake and metabolism because it can be blocked by inhibition of oxidative phosphorylation. Here, we extend these previous studies by analyzing, in GLUT2-null islets, glucose transporter isoforms and glucokinase expression and by measuring glucose usage, GSIS, and glucose-stimulated insulin mRNA biosynthesis. We show that in the absence of GLUT2, no compensatory expression of either GLUT1 or GLUT3 is observed and that glucokinase is expressed at normal levels. Glucose usage by isolated islets was increased between 1 and 6 mmol/l glucose but was not further increased between 6 and 20 mmol/l glucose. Parallel GSIS measurements showed that insulin secretion was not stimulated between 2.8 and 6 mmol/l glucose but was increased by >4-fold between 6 and 20 mmol/l glucose. Stimulation by glucose of total protein and insulin biosynthesis was also markedly impaired in the absence of GLUT2. Finally, we re-expressed GLUT2 in GLUT2-null beta-cells using recombinant lentiviruses and demonstrated a restoration of normal GSIS. Together, these data show that in the absence of GLUT2, glucose can still be taken up by beta-cells, albeit at a low rate, and that this transport activity is unlikely to be attributed to GLUT1 or GLUT3. This uptake activity, however, is limiting for normal glucose utilization and signaling to secretion and translation. These data further demonstrate the key role of GLUT2 in murine beta-cells for glucose signaling to insulin secretion and biosynthesis.

Calcium Microdomains Control Exo-Endocytosis of Synaptic-Like Microvesicles in Astrocytes

During the last decade, the discovery that astrocytes possess a nonelectrical form of excitability (Ca21-excitability) that leads to the release of chemical transmitters, an activity called ''gliotransmission'', indicates that these cells may have additional important roles in brain function. Elucidating the stimulus-secretion coupling leading to the exocytic release of chemical transmitters (such as glutamate, Bezzi et al., Nature Neurosci, 2004) may therefore clarify i) whether astrocytes represent in full a new class of secretory cells in the brain and ii) whether they can participate to the fast brain signaling in the brain. Here by using a recently developed approach for studying vesicle recycling dynamics at synapses (Voglmaier et al., Neuron, 2006; Balaji and Ryan, PNAS, 2007) combined with epifluorescence and total internal reflection fluorescence (TIRF) imaging, we investigated the spatiotemporal characteristics of stimulus-secretion coupling leading glutamate exocytosis of synaptic-like microvesicles (SLMVs) in astrocytes. We performed the analysis at both the whole-cell and single-vesicle levels providing the first system for comparing exo-endocytic processes in astrocytes with those in neurons. Both the time course and modalities of secretion in astrocytes present more similarities to neurons then previously expected. We found that 1. the G-protein-coupled receptor (GPCR)-evoked exocytosis reached the maximum on a ms time scale and that 2. ER tubuli formed sub-micrometer domains beneath the plasma membrane in close proximity to exocytic vesicles, where fusion events were spatiotemporally correlated with fast Ca21 events.