Neutron spectrometer for fast nuclear reactors

In this paper we describe the development and first tests of a neutron spectrometer designed for high flux environments, such as the ones found in fast nuclear reactors. The spectrometer is based on the conversion of neutrons impinging on $^6$Li into $\alpha$ and $t$ whose total energy comprises the initial neutron energy and the reaction $Q$-value. The $^6$LiF layer is sandwiched between two CVD diamond detectors, which measure the two reaction products in coincidence. The spectrometer was calibrated at two neutron energies in well known thermal and 3 MeV neutron fluxes. The measured neutron detection efficiency varies from 4.2$\times 10^{-4}$ to 3.5$\times 10^{-8}$ for thermal and 3 MeV neutrons, respectively. These values are in agreement with Geant4 simulations and close to simple estimates based on the knowledge of the $^6$Li(n,$\alpha$)$t$ cross section. The energy resolution of the spectrometer was found to be better than 100 keV when using 5 m cables between the detector and the preamplifiers.Comment: submitted to NI

pGlu-serpinin protects the normotensive and hypertensive heart from ischemic injury

Serpinin peptides derive from proteolytic cleavage of Chromogranin-A at C-terminus. Serpinin and the more potent pyroglutaminated-Serpinin (pGlu-Serp) are positive cardiac beta-adrenergic-like modulators, acting through β1-AR/AC/cAMP/PKA pathway. Since in some conditions this pathway and/or other pro-survival pathways, activated by other Chromogranin-A fragments, may cross-talk and may be protective, here we explored whether pGlu-Serp cardioprotects against ischemia/reperfusion injury under normotensive and hypertensive conditions. In the latter condition cardioprotection is often blunted because of the limitations on pro-survival Reperfusion-Injury-Salvage-Kinases (RISK) pathway activation. The effects of pGlu-Serp were evaluated on infarct size (IS) and cardiac function by using the isolated and Langendorff perfused heart of normotensive (WKY) and spontaneously hypertensive (SHR) rats exposed to ischemic pre-conditioning (PreC) and post-conditioning (PostC). In both WKY and SHR rat, pGlu-Serp induced mild cardioprotection in both PreC and in PostC. pGlu-Serp administered at the reperfusion (Serp-PostC) significantly reduced IS, being more protective in SHR than in WKY. Conversely, developed Left Ventricular Pressure (LVDevP) post-ischemic recovery was greater in WKY than in SHR. pGlu-Serp-PostC reduced contracture in both strains. Co-infusion with specific RISK inhibitors (PI3K/AkT, MitoK(ATP) channels, and PKC) blocked the pGlu-Serp-PostC protective effects. To show direct effect on cardiomyocytes, we pre-treated H9c2 with pGlu-Serp which were thus protected against hypoxia/reoxygenation. These results suggest pGlu-Serp as a potential modulatory agent implicated in the protective processes which can limit infarct size and overcome the hypertension-induced failure of PostC

Platelet-Rich Plasma combined with a sterile 3D polylactic acid scaffold for postoperative management of complete hoof wall resection for keratoma in four horses.

Keratoma is a non-malignant horse tumour that grows in the space between the horn of the hoof and the distal phalanx. Keratoma causes lameness in the horse, and surgical excision is the treatment of choice. Four horses underwent removal of a keratoma by complete hoof wall resection. The remaining wound was treated with Platelet-Rich Plasma (PRP) combined with a sterile 3D polylactic acid scaffold. The PRP was applied at 3, 6, 9, 12, 15 and 18 days postoperatively. The surgical site was cleaned with gauzes and swabs soaked in Ringer’s lactate solution before applying PRP and the foot bandage. Healthy granulation tissue developed at 6-21 days postoperatively. The hoof wall defect was completely filled with new hoof wall within 6-8 months after surgery. All horses returned to their previous exercise level and no recurrence of lameness was reported by the owner

Catestatin Increases the Expression of Anti-Apoptotic and Pro-Angiogenetic Factors in the Post-Ischemic Hypertrophied Heart of SHR.

BACKGROUND:In the presence of comorbidities the effectiveness of many cardioprotective strategies is blunted. The goal of this study was to assess in a hypertensive rat model if the early reperfusion with anti-hypertensive and pro-angiogenic Chromogranin A-derived peptide, Catestatin (CST:hCgA352-372; CST-Post), protects the heart via Reperfusion-Injury-Salvage-Kinases (RISK)-pathway activation, limiting infarct-size and apoptosis, and promoting angiogenetic factors (e.g., hypoxia inducible factor, HIF-1α, and endothelial nitric oxide synthase, eNOS, expression). METHODS AND RESULTS:The effects of CST-Post on infarct-size, apoptosis and pro-angiogenetic factors were studied in isolated hearts of spontaneously hypertensive rats (SHR), which underwent the following protocols: (a) 30-min ischemia and 120-min reperfusion (I/R); (b) 30-min ischemia and 20-min reperfusion (I/R-short), both with and without CST-Post (75 nM for 20-min at the beginning of reperfusion). In unprotected Wistar-Kyoto hearts, used as normal counterpart, infarct-size resulted smaller than in SHR. CST-Post reduced significantly infarct-size and improved post-ischemic cardiac function in both strains. After 20-min reperfusion, CST-Post induced S-nitrosylation of calcium channels and phosphorylation of RISK-pathway in WKY and SHR hearts. Yet specific inhibitors of the RISK pathway blocked the CST-Post protective effects against infarct in the 120-min reperfusion groups. Moreover, apoptosis (evaluated by TUNEL, ARC and cleaved caspase) was reduced by CST-Post. Importantly, CST-Post increased expression of pro-angiogenetic factors (i.e., HIF-1α and eNOS expression) after two-hour reperfusion. CONCLUSIONS:CST-Post limits reperfusion damages and reverses the hypertension-induced increase of I/R susceptibility. Moreover, CST-Post triggers antiapoptotic and pro-angiogenetic factors suggesting that CST-Post can be used as an anti-maladaptive remodeling treatment

Network Physiology reveals relations between network topology and physiological function

The human organism is an integrated network where complex physiologic systems, each with its own regulatory mechanisms, continuously interact, and where failure of one system can trigger a breakdown of the entire network. Identifying and quantifying dynamical networks of diverse systems with different types of interactions is a challenge. Here, we develop a framework to probe interactions among diverse systems, and we identify a physiologic network. We find that each physiologic state is characterized by a specific network structure, demonstrating a robust interplay between network topology and function. Across physiologic states the network undergoes topological transitions associated with fast reorganization of physiologic interactions on time scales of a few minutes, indicating high network flexibility in response to perturbations. The proposed system-wide integrative approach may facilitate the development of a new field, Network Physiology.Comment: 12 pages, 9 figure