319 research outputs found
Modeling and Control of Quantum Systems: An Introduction
The scope of this work is to provide a self-contained introduction to a selection of basic theoretical aspects in the modeling and control of quantum mechanical systems, as well as a brief survey on the main approaches to control synthesis. While part of the existing theory, especially in the open-loop setting, stems directly from classical control theory (most notably geometric control and optimal control), a number of tools specifically tailored for quantum systems have been developed since the 1980s, in order to take into account their distinctive features: the probabilistic nature of atomic-scale physical systems, the effect of dissipation and the irreversible character of the measurements have all proved to be critical in feedback-design problems. The relevant dynamical models for both closed and open quantum systems are presented, along with the main results on their controllability and stability. A brief review of several currently available control design methods is meant to provide the interested reader with a roadmap for further studies
The role of bisphosphonates in the treatment of painful metastatic bone disease: A review of phase III trials
Metastatic bone disease is a frequent cause of morbidity in advanced cancer patients with a subsequent high incidence of skeletal complications (fractures, hypercalcemia, spinal cord compression) and severe pain. The osteolytic process is mainly characterized by an osteoclastic activity of bone resorption and inflammatory activity provoked by various cytokines and prostaglandins. Bisphosphonates represent a new class of drugs with inhibitory activity on bone resorption and on inflammatory processes which revealed themselves to be efficacious in a series of clinical conditions such as tumour-induced hypercalcemia, Paget's disease, osteoporosis and metastatic bone disease. The aim of this review of the literature is to show the analgesic efficacy of the different bisphosphonates in phase III studies carried out on patients with metastatic bone disease. Medline and Cancerlit database from January 1984 to February 1998 have been considered. From the analysis of the published studies it appears that bisphosphonates and, in particular, intravenous Disodium Pamidronate, are not only able to slow down the progression of the disease and to reduce the onset of skeletal complications but also have an analgesic effect and the possibility of improving the quality of life, above all in patients with osteolytic metastases due to breast cancer and multiple myeloma. Bisphosphonates represent a further valid therapy to add to an already consolidated list of therapies such as radio, chemo and endocrine therapy, analgesic drugs, orthopaedic and physiatric in the pain management of patients with bone metastases. These drugs meet with the patients' compliance, are well-tolerated as well as having a good cost/efficacy profile. It still remains to be seen if the newer and more potent bisphosphonates such as Ibandronate and Zoledronate can be administered differently from the intravenous route such as by mouth or by patch which are readily accepted by the patient and, moreover, if these more potent drugs are able to prevent or delay the onset and/or the progression of bone metastases. Copyright (C) 1998 International Association for the Study of Pain. Published by Elsevier Science B.V
Amyotrophic Lateral Sclerosis: Neurochemical Biomarkers
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of upper and lower motor neurons, causing relentless paralysis. There is a need for ALS biomarkers in order to facilitate early and differential diagnosis and prediction of disease course. The most promising ALS biomarkers are neurofilaments (phosphorylated heavy chain [pNFH] and light chain [NFL]), for which increasing evidence probably warrants their introduction in the clinical scenario in the near future. Their levels are raised in the CSF of ALS patients as a consequence of release from degenerating motor neuron axons, therefore enabling differentiation from most other conditions. Neurofilaments also have prognostic value, predicting survival and correlating with disease progression rate. Thanks to technological advances, neurofilaments can now be measured also in the blood, providing information which is similar to that given by their CSF counterparts. As neurofilament levels are stable over time and blood sampling makes longitudinal measurements easy, they are particularly promising as pharmacodynamic biomarkers for trials of experimental therapeutics. Another class of ALS biomarkers is that of neuroinflammatory molecules, among which the chitinases, and particularly chitotriosidase (Chit1), have been most studied in the last years. Though significantly raised in the CSF in ALS, the diagnostic performance of Chit1 is actually lower than that of neurofilaments; its potential usefulness is rather due to the fact that it presumably reflects microglial inflammation occurring in the non-cell-autonomous neurodegenerative process, which, together with the longitudinal stability of CSF levels, would enable its use as a pharmacodynamic biomarker in future trials targeting neuroinflammation
Stabilization of Stochastic Quantum Dynamics via Open- and Closed-Loop Control
In this paper, we investigate parametrization-free solutions of the problem of quantum pure state preparation and subspace stabilization by means of Hamiltonian control, continuous measurement, and quantum feedback, in the presence of a Markovian environment. In particular, we show that whenever suitable dissipative effects are induced either by the unmonitored environment, or by non-Hermitian measurements, there is no need for feedback, as open-loop time-invariant control is sufficient to achieve stabilization of the target set in probability. Constructive necessary and sufficient conditions on the form of the control Hamiltonian can be provided in this case. When time-invariant control is not sufficient, state stabilization can be attained by the addition of filtering-based feedback control
Amyotrophic lateral sclerosis: Epidemiology and risk factors
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease of motor neurons, invariably leading to progressive paralysis and death in 3–5 years from onset. ALS has an annual incidence of 2/100,000 and a prevalence of 6/100,000. The disease is more common in males and in Caucasian ethnicities and its incidence rises with advancing age. Age at onset and site of onset (bulbar vs. spinal) are the two main prognostic factors in ALS. The only certain risk factors for ALS are positive family history, male gender, and advancing age; among environmental factors, cigarette smoking is supported by the most robust evidence, whereas others are less well documented. However, most epidemiological studies on environmental risk factors in ALS are limited by methodological flaws. Future researches should be performed according to more stringent criteria and on larger cohorts, and they should also aim to capture the complex interplay between genetic and environmental factors in ALS pathogenesis
Investigation on the mechanisms involved in the central protective effect of amylin on gastric ulcers in rats
1. The mechanisms involved in the protective effect of amylin (administered into the brain ventricle, i.c.v.) on gastric ulcers induced by the oral administration of ethanol 50% (EtOH, 2 ml/rat) or indomethacin (indomethacin, 20 mg kg(-1), at a dosing volume of 5 ml) were investigated in rats. 2. The possible involvement of endogenous nitric oxide (NO) in the beneficial effect of amylin against EtOH-induced ulcers was examined. The inhibitor of NO-synthesis, NG-nitro-L-arginine methyl ester (L-NAME, 70 mg kg(-1), s.c.) was injected 30 min before amylin (2.2 microg/rat, i.c.v.) followed by EtOH after a further 30 min. Rats were sacrificed 1 h after EtOH. L-NAME completely removed the protective effect of amylin. 3. The interaction between amylin and gastric nonprotein sulfhydryl groups was studied. The rats were treated with N-ethyl-maleimide (NEM, 25 mg kg(-1), s.c.) 30 min before amylin (2.2 microg/rat, i.c.v.) followed by EtOH 30 min after or by indomethacin 5 min after amylin. Rats were sacrificed 1 h or 6 h respectively after EtOH or indomethacin. NEM counteracted the protective effect of amylin against EtOH-induced ulcers but not against those provoked by indomethacin. 4. To determine whether amylin was able to promote ulcer healing, the peptide was injected 5 min after EtOH or 1 h after indomethacin. In the case of EtOH, the beneficial effect of amylin was lost whereas it was still effective on indomethacin-induced ulcers. 5. The results indicate that: the mechanisms involved in the antiulcer effects of amylin are different in these two types of gastric lesions probably because of the different etiopathology of various types of ulcers. Endogenous NO and nonprotein sulfhydryl groups are involved in the mucosal protective effects of amylin on EtOH and not on indomethacin-induced ulcers. Furthermore the effectiveness of amylin against indomethacin-induced lesions when administered after the ulcerogenic process has started suggests that amylin is involved not only in the protection but also in the healing mechanisms in this type of ulcer
Amyotrophic lateral sclerosis: Genotypes and phenotypes
Mendelian forms of amyotrophic lateral sclerosis (ALS) account for nearly 10 % of all cases. To date, 19 disease genes, usually but not exclusively inherited with an autosomal dominant pattern, have been reported to be associated with ALS or with atypical motor neuron diseases with or without associated frontotemporal dementia (ALS-FTD). Often, it is possible to draw correlations between distinct ALS-associated mutations and specifi c clinical phenotypes. This information is essential for biologists and clinicians alike, providing at the same time an unparalleled insight into the pathogenesis of the disease and invaluable tools for genetic counseling, diagnosis, and development of preventive strategies and treatments for ALS
Advance care planning and mental capacity in ALS: a current challenge for an unsolved matter
La diagnosi di Sclerosi Laterale Amiotrofica(SLA): 2009
The diagnosis of ALS per se may be challenging since there is no single diagnostic test for the disease with the exception, today, of finding a mutation in defined genes as SOD1, TDP-43, etc. The World Federation of Neurology (WFN) developed workable, internationally acceptable diagnostic criteria that would enhance clinical and research studies in the field of ALS. The revised El Escorial criteria edited in 2000 (Brooks et al., 2000) state that to establish the diagnosis of ALS, a combination of LMN and UMN signs with evidence of spread is required. Four cardinal regions have been defined and spread of signs from region to region is essential for the character of ALS. On clinical ground it is seldom possible to establish an early diagnosis of ALS that needs then to be supported mainly by neurophysiological testing. In clinical practice the differential diagnosis of ALS is extensive because symptoms and signs of both LMN and UMN are encountered in a large and varied group of disorders, both neurologic and systemic. Furthermore, today two areas deserve particular attention in the process of diagnosis: cognitive impairments once considered rare or uncommon occur in a large percentage of ALS patients. Careful neuropsychological testing needs indeed to be completed for possible overlapping forms with fronto-temporal dementia (FTDL). Furthermore, the most intriguing area is related to genetics. Since 1993 and the definition of SOD1 mutations in familial ALS, other genes have been discovered and the impact of genetics on ALS diagnosis is today critical. An accurate understanding of the familial contribution to ALS would have a significant impact on the diagnosis of individuals both at an early age, prior to the onset of symptoms or at the first appearance of symptoms. In practice, the diagnosis of any is made by a process of clinic logic that is defined both by the characteristics of the disease itself and by an intuitive process of decision making in which the clinician weights the clinical evidence according to an experiential model built from clinical experience gained over time. In ALS, this concept must be revisited because the recent impact of new genetic discoveries requires to the clinician a continuous update for the genotype-clinical phenotype coupling. New genetic acquisitions can unquestionably speed early diagnosis of ALS
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