Quasi 1D modelling of a Scramjet engine cycle using Heiser-Pratt approach

Scramjet engines are key for sustained hypersonic flights. Analytic models play a critical role in the preliminary design of a scramjet engine configuration. The objective of this research is to develop and validate a quasi-1D model for the scramjet engine encompassing inlet, isolator and combustor, to evaluate the impact of flight conditions and design parameters on the engine functionality. The model is developed assuming isentropic flow in the inlet with a single turn; modified Fanno-flow equations in the isolator that account for the area change of the core flow; and the combustor is modeled using Heiser-Pratt equations accounting for the fuel mixing efficiency. The isolator and combustor models are validated against experimental results. The model accounts for twelve parameters allowing for a decent range of possible configurations. Finally, the model was applied to five sets of parametric studies to evaluate the effect of multiple parameters on the engine functionality

Characterization of cancer - associated adipose tissue.

A large body of evidences has contributed to establish a strict association between adipose tissue and cancer in the contest of metabolic disorders such as obesity. Epidemiological studies have shown that obese patients have a drastically higher risk to develop cancer. This tumor-promoting role in the context of obesity is thought to rely mainly on the aberrant systemic and paracrine release of pro-inflammatory cytokines by fat cells, which ultimately cooperate to boost cancer cell proliferation and metastatic dissemination. In addition, cancer associated adipocytes (CAAs) may contribute in tumor progression by providing a metabolic support to the aberrant bioenergetics demand of cancer cells. However, it still remains to be established whether a relevant pro-inflammatory effect might be exerted by peritumoral adipose tissue in non-obese patients with gastrointestinal cancer. Gastrointestinal cancers are responsible for more deaths than any other cancer in the body. As for other types of cancer, many studies have revealed the strong relationship between gastrointestinal neoplasms and systemic disorders of adipose tissue, such as obesity and diabetes, but almost nothing is known about the local interaction between gastrointestinal cancer cells and peritumoral adipocytes in non-obese/non-diabetic patients. In order to start bridge this gap we assess whether adipose tissue surrounding human gastrointestinal tumors might be altered in terms of adipocyte morphology and inflammatory infiltration. Specifically we compare peritumoral and non-peritumoral adipose tissue (visceral fat distant from tumor lesion) for the adipocyte size and morphology, cell count of lymphocytes (CD3 positive cells, CD3+) and macrophages (CD68 positive cells, CD68+). We found that peritumoral adipose tissue exhibit significantly reduced adipocyte size and increased number of activated lymphocytes and macrophages. Our results provide clinical evidences in support of the emerging notion that adipocytes at the tumor-stroma interface participate in a highly complex vicious cycle organized by cancer cells to promote tumor progression. Specifically our results suggest that peritumoral adipocytes might provide a significant contribution to enhance tumor burden by fueling cancer cell's metabolic demands and providing mitogenic signals via the paracrine release of pro-inflammatory cytokines. \u200

Does Pilocarpine-Induced Epilepsy in Adult Rats Require Status epilepticus?

Pilocarpine-induced seizures in rats provide a widely animal model of temporal lobe epilepsy. Some evidences reported in the literature suggest that at least 1 h of status epilepticus (SE) is required to produce subsequent chronic phase, due to the SE-related acute neuronal damage. However, recent data seems to indicate that neuro-inflammation plays a crucial role in epileptogenesis, modulating secondarily a neuronal insult. For this reason, we decided to test the following hypotheses: a) whether pilocarpine-injected rats that did not develop SE can exhibit long-term chronic spontaneous recurrent seizures (SRS) and b) whether acute neurodegeneration is mandatory to obtain chronic epilepsy. Therefore, we compared animals injected with the same dose of pilocarpine that developed or did not SE, and saline treated rats. We used telemetric acquisition of EEG as long-term monitoring system to evaluate the occurrence of seizures in non-SE pilocarpineinjected animals. Furthermore, histology and MRI analysis were applied in order to detect neuronal injury and neuropathological signs. Our observations indicate that non-SE rats exhibit SRS almost 8 (+/22) months after pilocarpine-injection, independently to the absence of initial acute neuronal injury. This is the first time reported that pilocarpine injected rats without developing SE, can experience SRS after a long latency period resembling human pathology. Thus, we strongly emphasize the important meaning of including these animals to model human epileptogenesis in pilocarpine induced epilepsy

A role for leukocyte-endothelial adhesion mechanisms in epilepsy

The mechanisms involved in the pathogenesis of epilepsy, a chronic neurological disorder that affects approximately 1 percent of the world population, are not well understood1–3. Using a mouse model of epilepsy, we show that seizures induce elevated expression of vascular cell adhesion molecules and enhanced leukocyte rolling and arrest in brain vessels mediated by the leukocyte mucin P-selectin glycoprotein ligand-1 (PSGL-1) and leukocyte integrins α4β1 and αLβ2. Inhibition of leukocyte-vascular interactions either with blocking antibodies, or in mice genetically deficient in functional PSGL-1, dramatically reduced seizures. Treatment with blocking antibodies following acute seizures prevented the development of epilepsy. Neutrophil depletion also inhibited acute seizure induction and chronic spontaneous recurrent seizures. Blood-brain barrier (BBB) leakage, which is known to enhance neuronal excitability, was induced by acute seizure activity but was prevented by blockade of leukocyte-vascular adhesion, suggesting a pathogenetic link between leukocyte-vascular interactions, BBB damage and seizure generation. Consistent with potential leukocyte involvement in the human, leukocytes were more abundant in brains of epileptics than of controls. Our results suggest leukocyte-endothelial interaction as a potential target for the prevention and treatment of epilepsy

MRI (T2 and rCBV) and histological (low-power vs higher magnifications) data are presented.

<p>The three histological areas used for the cell density evaluation reported above are, respectively, cerebral cortex, pyramidal layer of CA1 and hilus of the dentate gyrus.</p

Bar graphs for rCBV values in the same brain areas that were identified for T2 analysis.

<p>Bar graphs for rCBV values in the same brain areas that were identified for T2 analysis.</p

Bar graphs for T2 ratio in different brain areas.

<p>T2 ratio was calculated dividing T2 values for each region of interest (ROI) for the baseline (muscle levels). Data were evaluated with one-way analysis of variance (ANOVA), following LSD post-hoc test, setting the significance at p<.05.</p

A role for leukocyte-endothelial adhesion mechanisms in epilepsy

The mechanisms involved in the pathogenesis of epilepsy, a chronic neurological disorder that affects approximately 1 percent of the world population, are not well understood(1–3). Using a mouse model of epilepsy, we show that seizures induce elevated expression of vascular cell adhesion molecules and enhanced leukocyte rolling and arrest in brain vessels mediated by the leukocyte mucin P-selectin glycoprotein ligand-1 (PSGL-1) and leukocyte integrins α4β1 and αLβ2. Inhibition of leukocyte-vascular interactions either with blocking antibodies, or in mice genetically deficient in functional PSGL-1, dramatically reduced seizures. Treatment with blocking antibodies following acute seizures prevented the development of epilepsy. Neutrophil depletion also inhibited acute seizure induction and chronic spontaneous recurrent seizures. Blood-brain barrier (BBB) leakage, which is known to enhance neuronal excitability, was induced by acute seizure activity but was prevented by blockade of leukocyte-vascular adhesion, suggesting a pathogenetic link between leukocyte-vascular interactions, BBB damage and seizure generation. Consistent with potential leukocyte involvement in the human, leukocytes were more abundant in brains of epileptics than of controls. Our results suggest leukocyte-endothelial interaction as a potential target for the prevention and treatment of epilepsy