Reduced SL(2,R) WZNW Quantum Mechanics

The $SL(2,\R)$ WZNW $\rightarrow$ Liouville reduction leads to a nontrivial phase space on the classical level both in $0+1$ and $1+1$ dimensions. To study the consequences in the quantum theory, the quantum mechanics of the $0+1$ dimensional, point particle version of the constrained WZNW model is investigated. The spectrum and the eigenfunctions of the obtained---rather nontrivial---theory are given, and the physical connection between the pieces of the reduced configuration space is discussed in all the possible cases of the constraint parameters.Comment: LaTeX file, 33 pages. Results extended, contains all technical information not detailed in version to appear in J. Math. Phy

Spectral Structure of Quantum Line with a Defect

We study the spectral properties of one-dimensional quantum wire with a single defect. We reveal the existence of the non-trivial topological structures in the spectral space of the system, which are behind the exotic quantum phenomena that have lately been found in the system.Comment: 4 pages, LaTeX, To appear in Proc. International Symposium on Foundation of Quantum Mechanics, Tokyo, Aug.26-30, 2001 (ISQM-Tokyo 01

Is Aging Biology Ageist?

Abstract : The scientific questions we pursue are shaped by our cultural assumptions and biases, often in ways we are unaware. Here, we argue that modern biases against older adults (ageism) have unconsciously led aging biologists to assume that traits of older individuals are negative and those of younger individuals positive. We illustrate this bias with the example of how a medieval Chinese scholar might have approached the task of understanding aging biology. In particular, aging biologists have tended to emphasize functional declines during aging, rather than biological adaptation and population selection or composition processes; the reality is certainly that all these processes interact. Failure to make these distinctions could lead to interventions that improve superficial markers of aging while harming underlying health, particularly as the health priorities of older adults (autonomy, function, freedom from suffering, etc.) are often quite different from the goals of aging biologists (reducing disease, prolonging life). One approach to disentangling positive, negative, and neutral changes is to map trajectories of change across the life course of an individual (physiobiography). We emphasize that our goal is not to criticize our colleagues—we have been guilty too—but rather to help us all improve our science

Frailty in older people living with HIV: current status and clinical management

This paper will update care providers on the clinical and scientific aspects of frailty which affects an increasing proportion of older people living with HIV (PLWH). The successful use of combination antiretroviral therapy has improved long-term survival in PLWH. This has increased the proportion of PLWH older than 50 to more than 50% of the HIV population. Concurrently, there has been an increase in the premature development of age-related comorbidities as well as geriatric syndromes, especially frailty, which affects an important minority of older PLWH. As the number of frail older PLWH increases, this will have an important impact on their health care delivery. Frailty negatively affects a PLWH's clinical status, and increases their risk of adverse outcomes, impacting quality of life and health-span. The biologic constructs underlying the development of frailty integrate interrelated pathways which are affected by the process of aging and those factors which accelerate aging. The negative impact of sarcopenia in maintaining musculoskeletal integrity and thereby functional status may represent a bidirectional interaction with frailty in PLWH. Furthermore, there is a growing body of literature that frailty states may be transitional. The recognition and management of related risk factors will help to mitigate the development of frailty. The application of interdisciplinary geriatric management principles to the care of older PLWH allows reliable screening and care practices for frailty. Insight into frailty, increasingly recognized as an important marker of biologic age, will help to understand the diversity of clinical status occurring in PLWH, which therefore represents a fundamentally new and important aspect to be evaluated in their health care

The role of the MAPK pathway alterations in GM-CSF modulated human neutrophil apoptosis with aging

BACKGROUND: Neutrophils represent the first line of defence against aggressions. The programmed death of neutrophils is delayed by pro-inflammatory stimuli to ensure a proper resolution of the inflammation in time and place. The pro-inflammatory stimuli include granulocyte-macrophage colony-stimulating factor (GM-CSF). Recently, we have demonstrated that although neutrophils have an identical spontaneous apoptosis in elderly subjects compared to that in young subjects, the GM-CSF-induced delayed apoptosis is markedly diminished. The present study investigates whether an alteration of the GM-CSF stimulation of MAPKs play a role in the diminished rescue from apoptosis of PMN of elderly subjects. METHODS: Neutrophils were separated from healthy young and elderly donors satisfying the SENIEUR protocol. Neutrophils were stimulated with GM-CSF and inhibitors of the MAPKinase pathway. Apoptosis commitment, phosphorylation of signaling molecules, caspase-3 activities as well as expression of pro- and anti-apoptotic molecules were performed in this study. Data were analyzed using Student's two-tailed t-test for independent means. Significance was set for p ≤ 0.05 unless stated otherwise. RESULTS: In this paper we present evidence that an alteration in the p42/p44 MAPK activation occurs in PMN of elderly subjects under GM-CSF stimulation and this plays a role in the decreased delay of apoptosis of PMN in elderly. We also show that p38 MAPK does not play a role in GM-CSF delayed apoptosis in PMN of any age-groups, while it participates to the spontaneous apoptosis. Our results also show that the alteration of the p42/p44 MAPK activation contributes to the inability of GM-CSF to decrease the caspase-3 activation in PMN of elderly subjects. Moreover, GM-CSF converts the pro-apoptotic phenotype to an anti-apoptotic phenotype by modulating the bcl-2 family members Bax and Bcl-xL in PMN of young subjects, while this does not occur in PMN of elderly. However, this modulation seems MAPK independent. CONCLUSION: Our results show that the alteration of p42/p44 MAPK activation contributes to the GM-CSF induced decreased PMN rescue from apoptosis in elderly subjects. The modulation of MAPK activation in PMN of elderly subjects might help to restore the functionality of PMN with aging