The steady state quantum statistics of a non-Markovian atom laser

We present a fully quantum mechanical treatment of a single-mode atomic cavity with a pumping mechanism and an output coupling to a continuum of external modes. This system is a schematic description of an atom laser. In the dilute limit where atom-atom interactions are negligible, we have been able to solve this model without making the Born and Markov approximations. When coupling into free space, it is shown that for reasonable parameters there is a bound state which does not disperse, which means that there is no steady state. This bound state does not exist when gravity is included, and in that case the system reaches a steady state. We develop equations of motion for the two-time correlation in the presence of pumping and gravity in the output modes. We then calculate the steady-state output energy flux from the laser.Comment: 14 pages (twocloumn), 6 figure

Temporal fluctuations of waves in weakly nonlinear disordered media

We consider the multiple scattering of a scalar wave in a disordered medium with a weak nonlinearity of Kerr type. The perturbation theory, developed to calculate the temporal autocorrelation function of scattered wave, fails at short correlation times. A self-consistent calculation shows that for nonlinearities exceeding a certain threshold value, the multiple-scattering speckle pattern becomes unstable and exhibits spontaneous fluctuations even in the absence of scatterer motion. The instability is due to a distributed feedback in the system "coherent wave + nonlinear disordered medium". The feedback is provided by the multiple scattering. The development of instability is independent of the sign of nonlinearity.Comment: RevTeX, 15 pages (including 5 figures), accepted for publication in Phys. Rev.

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

Control of mitochondrial physiology and cell death by the Bcl-2 family proteins Bax and Bok

Neuronal cell death is often triggered by events that involve intracellular increases in Ca(2+). Under resting conditions, the intracellular Ca(2+) concentration is tightly controlled by a number of extrusion and sequestering mechanisms involving the plasma membrane, mitochondria, and ER. These mechanisms act to prevent a disruption of neuronal ion homeostasis. As these processes require ATP, excessive Ca(2+) overloading may cause energy depletion, mitochondrial dysfunction, and may eventually lead to Ca(2+)-dependent cell death. Excessive Ca(2+) entry though glutamate receptors (excitotoxicity) has been implicated in several neurologic and chronic neurodegenerative diseases, including ischemic stroke, epilepsy, and Alzheimer\u27s disease. Recent evidence has revealed that excitotoxic cell death is regulated by the B-cell lymphoma-2 (Bcl-2) family of proteins. Bcl-2 proteins, comprising of both pro-apoptotic and anti-apoptotic members, have been shown to not only mediate the intrinsic apoptosis pathway by controlling mitochondrial outer membrane (MOM) integrity, but to also control neuronal Ca(2+) homeostasis and energetics. In this review, the role of Bcl-2 family proteins in the regulation of apoptosis, their expression in the central nervous system and how they control Ca(2+)-dependent neuronal injury are summarized. We review the current knowledge on Bcl-2 family proteins in the regulation of mitochondrial function and bioenergetics, including the fusion and fission machinery, and their role in Ca(2+) homeostasis regulation at the mitochondria and ER. Specifically, we discuss how the \u27pro-apoptotic\u27 Bcl-2 family proteins, Bax and Bok, physiologically expressed in the nervous system, regulate such \u27non-apoptotic/daytime\u27 functions

Endocrine Aspects of Male Sexual Dysfunctions

Introduction. Endocrine disorders may adversely affect men's sexual function. Aim. To provide recommendations based on best evidence for diagnosis and treatment of endocrine-related male sexual dysfunctions. Methods. The Endocrine Aspects of Male Sexual Dysfunctions Committee, including 11 members from eight countries and four continents, collaborated with the Endocrine subcommittee of the Standards Committee of the International Society for Sexual Medicine. Medical literature was reviewed in detail, followed by extensive internal committee discussion over 2 years, then public presentation and discussion with the other experts before finalizing the report. Main Outcome Measure. Recommendations based on grading of evidence-base medical literature and interactive discussion. Results. From animal studies, it is derived that testosterone modulates mechanisms involved in erectile machinery, including expression of enzymes that both initiate and terminate erection. In addition, testosterone is essential for sexual motivation. Whether these findings could be extrapolated to human erections is unclear. Testosterone plays a broad role in men's overall health. Recent studies have established strong associations between low testosterone and metabolic and cardiovascular imbalances. In some studies, low testosterone decreased longevity; however, longitudinal studies do not support the predictive value of low testosterone for further cardiovascular events. The article proposes a standardized process for diagnosis and treatment of endocrine-related male sexual dysfunctions, updating the knowledge on testosterone and prostate safety. There is no compelling evidence that testosterone treatment causes prostate cancer or its progression in men without severe testosterone deficiency (TD). The possible roles of prolactin and thyroid hormones are also examined. Conclusions. Men with erectile dysfunction, hypoactive sexual desire and retarded ejaculation, as well as those with visceral obesity and metabolic diseases, should be screened for TD and treated. Prospective interventional studies are required before screening for TD in more conditions, including cardiovascular diseases, and considering correction as preventive medicine as much data suggests. Buvat J, Maggi M, Gooren L, Guay AT, Kaufman J, Morgentaler A, Schulman C, Tan HM, Torres LO, Yassin A, and Zitzmann M. Endocrine aspects of male sexual dysfunctions. © 2010 International Society for Sexual Medicine.SCOPUS: ar.jinfo:eu-repo/semantics/publishe