97 research outputs found
Descriptors for Pentane-2,4-dione and Its Derivatives
We have used equations for partition coefficients of compounds from water and the gas phase to various solvents to obtain descriptors for pentane-2,4-dione and 21 of its derivatives. These descriptors can then be used to estimate further partition coefficients into a wide variety of solvents. The descriptors also yield information about the properties of pentane-2,4-dione and its derivatives. Pentane-2,4-dione and its alkyl derivatives are quite polar, with substantial hydrogen bond basicity but with no hydrogen bond acidity. In contrast 1,1,1-trifluoropentane-2,4-dione and hexafluoropentan-2,4-dione have significant hydrogen bond acidities
A proposed methodology for deriving tsunami fragility functions for buildings using optimum intensity measures
ERYTHROPOIETIN FOR THE TREATMENT OF SUBARACHNOID HEMORRAGE: A FEASIBLE INGREDIENT FOR A SUCCESS MEDICAL RECIPE
Subaracnhoid hemorrage (SAH) following aneurysm bleeding accounts for 6% to 8% of all cerebrovascular accidents. Althoug an aneurysm can be effectively managed by surgery or endovascular therapy, delayed cerebral ischemia is diagnosed in a high percentage of patients resulting in significant morbility and mortality. Cerebral vasospasm occurs in more than half of all patients after aneurysm rupture and is recognized as the leading cause of delayed cerebral ischemia after SAH. Hemodynamic strategies and endovascular procedures may be considered fo the treatment of cerebral vasospasm. In recent years, the mechanism contributing to the development of vasospasm, abnormal reactivity of cerebral arteries and cerebral ischemia following SAH, have been intensively investigated. A number of pathological processes have been identified in the pathogenesis of vasospasm including endothelial injury, smooth muscle cell contraction from spasmogenic substances produced by the subarachnoid blood clots, changes in vascular responsiveness and inflammatory response of the vascular endothelium. to date, the current therapeutic interventions remain ineffective being limited to the manipulation os systemic blood pressure, variation of blood volume and viscosity, and control of arterial carbon dioxide tension. In this scenario, the hormone erythropoietin (EPO), has been found to exert neuroprotective action during experimental SAH when its recombinant form (rHuEPO) is systematically administered. However, recent translation of experimental data into clinical trials has suggested an unclear role of recombinant human EPO in the setting of SAH. In this context, the aim of the recurrent review is to present current evidence on the potential role of EPO in cerebrovascular dysfunction following aneurysmal subarachnoid hemorrage
Erythropoietin: a multimodal neuroprotective agent
The tissue protective functions of the hematopoietic growth factor erythropoietin (EPO) are independent of its action on erythropoiesis. EPO and its receptors (EPOR) are expressed in multiple brain cells during brain development and upregulated in the adult brain after injury. Peripherally administered EPO crosses the blood-brain barrier and activates in the brain anti-apoptotic, anti-oxidant and anti-inflammatory signaling in neurons, glial and cerebrovascular endothelial cells and stimulates angiogenesis and neurogenesis. These mechanisms underlie its potent tissue protective effects in experimental models of stroke, cerebral hemorrhage, traumatic brain injury, neuroinflammatory and neurodegenerative disease. The preclinical data in support of the use of EPO in brain disease have already been translated to first clinical pilot studies with encouraging results with the use of EPO as a neuroprotective agent
Pharmacological treatment of delayed cerebral ischemia and vasospasm in subarachnoid hemorrhage
Subarachnoid hemorrhage after the rupture of a cerebral aneurysm is the cause of 6% to 8% of all cerebrovascular accidents involving 10 of 100,000 people each year. Despite effective treatment of the aneurysm, delayed cerebral ischemia (DCI) is observed in 30% of patients, with a peak on the tenth day, resulting in significant infirmity and mortality. Cerebral vasospasm occurs in more than half of all patients and is recognized as the main cause of delayed cerebral ischemia after subarachnoid hemorrhage. Its treatment comprises hemodynamic management and endovascular procedures. To date, the only drug shown to be efficacious on both the incidence of vasospasm and poor outcome is nimodipine. Given its modest effects, new pharmacological treatments are being developed to prevent and treat DCI. We review the different drugs currently being tested
Assessment of tsunami hazards in ports and their impact on marine vessels derived from tsunami models and the observed damage data
Experimental anticancer studies. Xxi. Effect of penicillin treatment of hemolytic streptococcus on its anticancer activity.
Hyperfine structure changes in iron-base amorphous alloys produced by high current density electropulsing
Experimental anticancer studies. XX. Effect of live hemolytic strep- tococci, grown in ribonucleic acid-containing broth, on tumor cells.
Developing fragility functions for the areas affected by the 2009 Samoa earthquake and tsunami
Fragility functions in terms of flow depth, flow velocity and hydrodynamic
force are developed to evaluate structural vulnerability in the areas
affected by the 2009 Samoa earthquake and tsunami. First, numerical
simulations of tsunami propagation and inundation are conducted to reproduce
the features of tsunami inundation. To validate the results, flow depths
measured in field surveys and waveforms measured by Deep-ocean Assessment and
Reporting of Tsunamis (DART) gauges are utilized. Next, building damage is
investigated by visually interpreting changes between pre- and post-tsunami
high-resolution satellite images. Finally, the data related to tsunami
features and building damage are integrated using Geographic Information System (GIS), and tsunami fragility functions are developed based on the
statistical analyses. From the developed fragility functions, we
quantitatively understood the vulnerability of a coastal region in American
Samoa characterized by steep terrains and ria coasts
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