Agreed-upon procedures report on the City of Martensdale, Iowa for the period July 1, 2014 through June 30, 2015

Agreed-upon procedures report on the City of Martensdale, Iowa for the period July 1, 2014 through June 30, 2015

Le Roman de Renart

F. 1-48. Le Roman de Renart. Le manuscrit, qui a été doté du sigle O dans les différentes éditions, est incomplet de la fin et mixte, proposant une structure relativement inédite. Il a récemment fait l’objet d’une édition critique par Aurélie Barre : Édition critique et littéraire du manuscrit O du « Roman de Renart » ( f. fr. 12583), doctorat, Université Lyon III, 2005. F. 1a-14b. Branche I.F. 1a-7e. [Branche Ia : « Le jugement de Renart »]. « Pierres qui son enging et s’art / Mist es vers faire de Renart…-… Tant qu’il [re]fu en sa santé / Com il avoit devant esté ». – F. 7e-10b. [Branche Ib : « Le Siège de Maupertuis »]. « Messires Nobles l’empereres / Vint au chastel ou Renart ere …-… Et Renart ainsi s’en eschape, / Des or gart bien chascun sa chape ! ». – F. 10b-14b. [Branche Ic : « Renart teinturier, Renart jongleur »]. « Li rois a fait son ban crier, / Par tout plevir et afier …-… Puis fu Renart lonc tens en mue ; / Ne va, ne vient, ne se remue » (éd. Barre, p.117-233, v. 1-3217). . F. 14b-20bBranche II. F. 14b-20b. [Branche II : « Le duel judiciaire »]. « Messires Nobles li lions / O lui avoit toz ses barons …-… Et autre redirai aprés, / A itant de cestui vos lés » (éd. Barre, p. 235-289, v. 1-1522). F. 20b-25c. Branche III.F. 20b-22a. [Branche IIIa : « Renart et Chantecler »]. « Seignors, oï avez maint conte, / Que maint contierres vos aconte …-… Dou coc qui li est eschapez, / Quant il ne s’en est saoulez ». – F. 22a-22f. [Branche IIIb : « Renart et la mésange »]. « Que que cil se plaint et demente, / Atant es vos une mesenge …-… Assez a grant travail eü / de ce dont li est mescheü ». – F. 22f-23c. [Branche IIIc. « Renart et Tibert »]. « Que qu’il se plaint de s’aventure, / Qui li avient et pesme et dure …-… Tornez s’en est a mout grant paine …-… Si com aventure le maine ». – F. 23c-24e. [Branche IIId : « Renart et l’andouille »]. «Renart qui mout sot de treslüe, / Et qui mout ot grant fain eüe …-… Esfondree ert entr’eus la guerre, / Mes ne velt trive ne pes querre ». – F. 24e-25c. [Branche IIIe : « Tibert et les deux prêtres »]. « Thibert li chaz, dont je a dit, / Doute Renart assez petit …-… Qui touz nos a enfantosmez : / A paine en sui vis eschapez ! » (éd. Barre, p. 291-340, v. 1-1265). F. 25c-27d. Branche IV. F. 25c-26a. [Branche IVa : « Renart et Tiercelin »]. « Entre .II. mons, en une plangne / Tout droit au pié d’une montaigne …-… Fuiant s’en va les sauz menuz : / Ses anemis a confonduz ». – F. 26a-27d. [Branche IVb : « Le viol d’Hersent »]. « Cis plaiz fu ainsi deffinez / Et Renars s’est acheminez …-… Et est venuz a sa mesnie / Qui soz la roche est entasnie » (éd. Barre, p. 341-359, v. 1-524). F. 27d-29d. Branche V. [« Renart et les anguilles »]. « Seignors, ce fu en cest termine / Que li douz tens d’esté decline …-…Que de Renart se vengera / Ne jamés jor ne l’amera » (éd. Barre, p. 361-378, v. 1-514). F. 29d-31e. Branche VI. [« Le puits »]. « Prime covient tel chose dire / Dont je vos puisse faire rire …-… Et il le puet prandre en sa marge, / Sachiez qu’i li fera domage ! » (éd. Barre, p. 379-396, v. 1-537).. 31e-39c. Branche VII. F. 31e-32e. [Branche VIIa : « Le jambon enlevé »]. « [U]n jour issit hors de la lande / Isengrins por querre viande …-… .XV. jours va a grant baudour, / Onques Renars n’i fist sejour ». – F. 32c-32e. [Branche VIIb : « Renart et le grillon »]. « Renart s’en va tout son chemin. / Or veut (en) engignier Isengrin …-… Tornez s’en est grant aleüre / Et vet aillors querre droiture ». – F. 32e-36e. [Branche VIIc : « L’Escondit »]. « Atant s’apense d’une chose / Dont il sa fame sovent chose …-…Tant defoulé et tant batu / Qu’a Malpertuis l’ont enbatu ». – F. 36e-39c. [Branche VIId : « La confession de Renart »]. « Foux est qui croit sa male pense : / Mout remaint de ce que fox panse …-…L’escofle lor donne a mengier, / Qu’il en avoient grant mestier (éd. Barre, p. 397-470, v. 1-1960). F. 36c-48e. Branche VIII. [« Renart et Liétart »]. « Uns prestres de la Croiz en Brie, / Que Damediex doint bone vie …-… Ou au chiés ou a la parclose, / Qui n’est aüsés de la chose » (éd. Barre, p. 471-554, v. 1-2470). F. 48e. Branche IX (v. 1-86). [« Les Vêpres de Tibert »]. « Oiez une novele estoire / Qui bien doit estre en mémoire …-… Jel conterai a Hameline, / La foi et la reconnoissance… » (éd. Barre, p. 555-557, v. 1-85).

Report on a special investigation of the City of Lakota for the period July 1, 2013 through May 31, 2015

Report on a special investigation of the City of Lakota for the period July 1, 2013 through May 31, 2015

Agreed-upon procedures report on the City of Moravia, Iowa for the period July 1, 2014 through June 30, 2015

Agreed-upon procedures report on the City of Moravia, Iowa for the period July 1, 2014 through June 30, 2015

Improved SNR efficiency in gradient echo coronary MRA with high temporal resolution using parallel imaging.

Contemporary coronary magnetic resonance angiography techniques suffer from signal-to-noise ratio (SNR) constraints. We propose a method to enhance SNR in gradient echo coronary magnetic resonance angiography by using sensitivity encoding (SENSE). While the use of sensitivity encoding to improve SNR seems counterintuitive, it can be exploited by reducing the number of radiofrequency excitations during the acquisition window while lowering the signal readout bandwidth, therefore improving the radiofrequency receive to radiofrequency transmit duty cycle. Under certain conditions, this leads to improved SNR. The use of sensitivity encoding for improved SNR in three-dimensional coronary magnetic resonance angiography is investigated using numerical simulations and an in vitro and an in vivo study. A maximum 55% SNR enhancement for coronary magnetic resonance angiography was found both in vitro and in vivo, which is well consistent with the numerical simulations. This method is most suitable for spoiled gradient echo coronary magnetic resonance angiography in which a high temporal and spatial resolution is required.

Connexins: key mediators of endocrine function.

The appearance of multicellular organisms imposed the development of several mechanisms for cell-to-cell communication, whereby different types of cells coordinate their function. Some of these mechanisms depend on the intercellular diffusion of signal molecules in the extracellular spaces, whereas others require cell-to-cell contact. Among the latter mechanisms, those provided by the proteins of the connexin family are widespread in most tissues. Connexin signaling is achieved via direct exchanges of cytosolic molecules between adjacent cells at gap junctions, for cell-to-cell coupling, and possibly also involves the formation of membrane "hemi-channels," for the extracellular release of cytosolic signals, direct interactions between connexins and other cell proteins, and coordinated influence on the expression of multiple genes. Connexin signaling appears to be an obligatory attribute of all multicellular exocrine and endocrine glands. Specifically, the experimental evidence we review here points to a direct participation of the Cx36 isoform in the function of the insulin-producing β-cells of the endocrine pancreas, and of the Cx40 isoform in the function of the renin-producing juxtaglomerular epithelioid cells of the kidney cortex.

Initial results on in vivo human coronary MR angiography at 7 T.

Seven tesla (T) MR imaging is potentially promising for the morphologic evaluation of coronary arteries because of the increased signal-to-noise ratio compared to lower field strengths, in turn allowing improved spatial resolution, improved temporal resolution, or reduced scanning times. However, there are a large number of technical challenges, including the commercial 7 T systems not being equipped with homogeneous body radiofrequency coils, conservative specific absorption rate constraints, and magnified sample-induced amplitude of radiofrequency field inhomogeneity. In the present study, an initial attempt was made to address these challenges and to implement coronary MR angiography at 7 T. A single-element radiofrequency transmit and receive coil was designed and a 7 T specific imaging protocol was implemented, including significant changes in scout scanning, contrast generation, and navigator geometry compared to current protocols at 3 T. With this methodology, the first human coronary MR images were successfully obtained at 7 T, with both qualitative and quantitative findings being presented.

Urate-induced acute renal failure and chronic inflammation in liver-specific Glut9 knockout mice.

Plasma urate levels are higher in humans than rodents (240-360 vs. â^¼30 μM) because humans lack the liver enzyme uricase. High uricemia in humans may protect against oxidative stress, but hyperuricemia also associates with the metabolic syndrome, and urate and uric acid can crystallize to cause gout and renal dysfunctions. Thus, hyperuricemic animal models to study urate-induced pathologies are needed. We recently generated mice with liver-specific ablation of Glut9, a urate transporter providing access of urate to uricase (LG9KO mice). LG9KO mice had moderately high uricemia (â^¼120 μM). To further increase their uricemia, here we gavaged LG9KO mice for 3 days with inosine, a urate precursor; this treatment was applied in both chow- and high-fat-fed mice. In chow-fed LG9KO mice, uricemia peaked at 300 μM 2 h after the first gavage and normalized 24 h after the last gavage. In contrast, in high-fat-fed LG9KO mice, uricemia further rose to 500 μM. Plasma creatinine strongly increased, indicating acute renal failure. Kidneys showed tubule dilation, macrophage infiltration, and urate and uric acid crystals, associated with a more acidic urine. Six weeks after inosine gavage, plasma urate and creatinine had normalized. However, renal inflammation, fibrosis, and organ remodeling had developed despite the disappearance of urate and uric acid crystals. Thus, hyperuricemia and high-fat diet feeding combined to induce acute renal failure. Furthermore, a sterile inflammation caused by the initial crystal-induced lesions developed despite the disappearance of urate and uric acid crystals.

Treatment of brain metastases from non-small cell lung cancer with whole-brain radiotherapy (wbrt) in combination with gefitinib (gft) or temozolomide (tmz): a randomized multicenter phase ii trial of the swiss group of clinical cancer research (sakk #70/03)

BACKGROUND: Patients with BM rarely survive .6 months and are commonly excluded from clinical trials. We aimed at improving outcome by exploring 2 combined modality regimens with at the time novel agents for which single-agent activity had been shown. METHODS: NSCLC patients with multiple BM were randomized to WBRT (10 × 3 Gy) and either GFT 250 mg p.o. daily or TMZ 75 mg/m2 p.o. daily ×21/28 days, starting on Day 1 of RT and to be continued until PD. Primary endpoint was overall survival, a Simon's optimal 2-stage design was based on assumptions for the 3-month survival rate. Cognitive functioning and quality of life were also evaluated. RESULTS: Fifty-nine patients (36 M, 23 F; 9 after prior chemo) were included. Median age was 61 years (range 46-82), WHO PS was 0 in 18 patients, 1 in 31 patients, and 2 in 10 patients. All but 1 patients had extracranial disease; 33 of 43 (TMZ) and 15 of 16 (GFT) had adenocarcinoma histology. GFT arm was closed early after stage 1 analysis when the prespecified 3-mo survival rate threshold (66%) was not reached, causes of death were not GFT related. Main causes of death were PD in the CNS 24%, systemic 41%, both 8%, and toxicity 10% [intestinal perforation (2 patients), pneumonia (2), pulmonary emboli (1), pneumonitis NOS (1), seizure (1)]. We summarize here other patients' characteristics for the 2 trial arms: TMZ (n ¼ 43)/GFT (n ¼ 16); median treatment duration: 1.6 /1.8 mo; Grade 3-4 toxicity: lymphopenia 5 patients (12%)/0; fatigue 8 patients (19%)/2 patients (13%). Survival data for TMZ/GFT arms: 3-month survival rate: 58.1% (95% CI 42.1-73)/62.5% (95% CI 35- 85); median OS: 4.9 months (95% CI 2.5-5.6)/6.3 months (95% CI 2.2- 14.6); median PFS: 1.8 months (95% CI 1.5-1.8)/1.8 (95% CI 1.1-3.9); median time to neurol. progr.: 8.0 months (95% CI 2.2-X)/4.8 (95% CI 3.9-10.5). In a model to predict survival time including the variables' age, PS, number of BM, global QL, total MMSE score, and subjective cognitive function, none of the variables accounted for a significant improvement in survival time. CONCLUSIONS: The combinations of WBRT with GFT or TMZ were feasible. However, in this unselected patient population, survival remains poor and a high rate of complication was observed. Four patients died as a result of high-dose corticosteroids. Preliminary evaluation of cognitive function andQL failed to show significant improvement. Indications and patient selection for palliative treatment should be revisited and careful monitoring and supportive care is required. Research and progress for this frequent clinical situation is urgently needed. Trial partly supported by AstraZeneca (Switzerland), Essex Chemie (Switzerland) and Swiss Federal Government.

Study of fish swimming activity using Acoustical Doppler Velocimetry (ADV) techniques

Peer reviewed

Conditional maximum likelihood timing recovery: estimators and bounds

This paper is concerned with the derivation of new estimators and performance bounds for the problem of timing estimation of (linearly) digitally modulated signals. The conditional maximum likelihood (CML) method is adopted, in contrast to the classical low-SNR unconditional ML (UML) formulationthat is systematically applied in the literature for the derivationof non-data-aided (NDA) timing-error-detectors (TEDs). A new CML TED is derived and proved to be self-noise free, in contrast to the conventional low-SNR-UML TED. In addition, the paper provides a derivation of the conditional Cramér–Rao Bound (CRB ), which is higher (less optimistic) than the modified CRB (MCRB)[which is only reached by decision-directed (DD) methods]. It is shown that the CRB is a lower bound on the asymptotic statisticalaccuracy of the set of consistent estimators that are quadratic with respect to the received signal. Although the obtained boundis not general, it applies to most NDA synchronizers proposed in the literature. A closed-form expression of the conditional CRBis obtained, and numerical results confirm that the CML TED attains the new bound for moderate to high Eg/No.

Fetal programming of pulmonary vascular dysfunction in mice: role of epigenetic mechanisms.

Insults during the fetal period predispose the offspring to systemic cardiovascular disease, but little is known about the pulmonary circulation and the underlying mechanisms. Maternal undernutrition during pregnancy may represent a model to investigate underlying mechanisms, because it is associated with systemic vascular dysfunction in the offspring in animals and humans. In rats, restrictive diet during pregnancy (RDP) increases oxidative stress in the placenta. Oxygen species are known to induce epigenetic alterations and may cross the placental barrier. We hypothesized that RDP in mice induces pulmonary vascular dysfunction in the offspring that is related to an epigenetic mechanism. To test this hypothesis, we assessed pulmonary vascular function and lung DNA methylation in offspring of RDP and in control mice at the end of a 2-wk exposure to hypoxia. We found that endothelium-dependent pulmonary artery vasodilation in vitro was impaired and hypoxia-induced pulmonary hypertension and right ventricular hypertrophy in vivo were exaggerated in offspring of RDP. This pulmonary vascular dysfunction was associated with altered lung DNA methylation. Administration of the histone deacetylase inhibitors butyrate and trichostatin A to offspring of RDP normalized pulmonary DNA methylation and vascular function. Finally, administration of the nitroxide Tempol to the mother during RDP prevented vascular dysfunction and dysmethylation in the offspring. These findings demonstrate that in mice undernutrition during gestation induces pulmonary vascular dysfunction in the offspring by an epigenetic mechanism. A similar mechanism may be involved in the fetal programming of vascular dysfunction in humans.

In vivo nuclear translocation of mineralocorticoid and glucocorticoid receptors in rat kidney: differential effect of corticosteroids along the distal tubule.

Aldosterone and corticosterone bind to mineralocorticoid (MR) and glucocorticoid receptors (GR), which, upon ligand binding, are thought to translocate to the cell nucleus to act as transcription factors. Mineralocorticoid selectivity is achieved by the 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) that inactivates 11β-hydroxy glucocorticoids. High expression levels of 11β-HSD2 characterize the aldosterone-sensitive distal nephron (ASDN), which comprises the segment-specific cells of late distal convoluted tubule (DCT2), connecting tubule (CNT), and collecting duct (CD). We used MR- and GR-specific antibodies to study localization and regulation of MR and GR in kidneys of rats with altered plasma aldosterone and corticosterone levels. In control rats, MR and GR were found in cell nuclei of thick ascending limb (TAL), DCT, CNT, CD cells, and intercalated cells (IC). GR was also abundant in cell nuclei and the subapical compartment of proximal tubule (PT) cells. Dietary NaCl loading, which lowers plasma aldosterone, caused a selective removal of GR from cell nuclei of 11β-HSD2-positive ASDN. The nuclear localization of MR was unaffected. Adrenalectomy (ADX) resulted in removal of MR and GR from the cell nuclei of all epithelial cells. Aldosterone replacement rapidly relocated the receptors in the cell nuclei. In ASDN cells, low-dose corticosterone replacement caused nuclear localization of MR, but not of GR. The GR was redistributed to the nucleus only in PT, TAL, early DCT, and IC that express no or very little 11β-HSD2. In ASDN cells, nuclear GR localization was only achieved when corticosterone was replaced at high doses. Thus ligand-induced nuclear translocation of MR and GR are part of MR and GR regulation in the kidney and show remarkable segment- and cell type-specific characteristics. Differential regulation of MR and GR may alter the level of heterodimerization of the receptors and hence may contribute to the complexity of corticosteroid effects on ASDN function.