Pulse confinement in optical fibers with random dispersion

Short range correlated uniform noise in the dispersion coefficient, inherent in many types of optical fibers, broadens and eventually destroys all initially ultra-short pulses. However, under the constraint that the integral of the random component of the dispersion coefficient is set to zero, or pinned, periodically or quasi-periodically along the fiber, the nature of the pulse propagation changes dramatically. For the case that randomness is added to constant positive dispersion, the pinning restriction significantly reduces pulse broadening. If the randomness is added to piecewise constant periodic dispersion, the pinning may even provide probability distributions of pulse parameters that are numerically indistinguishable from the statistically steady case. The pinning method can be used to both manufacture better fibers and upgrade existing fiber links.Comment: 4 pages, 2 figure

Experimental Assessment of the Role of Acetaldehyde in Alcoholic Cardiomyopathy

Alcoholism is one of the major causes of non-ischemic heart damage. The myopathic state of the heart due to alcohol consumption, namely alcoholic cardiomyopathy, is manifested by cardiac hypertrophy, compromised ventricular contractility and cardiac output. Several mechanisms have been postulated for alcoholic cardiomyopathy including oxidative damage, accumulation of triglycerides, altered fatty acid extraction, decreased myofilament Ca(2+ )sensitivity, and impaired protein synthesis. Despite intensive efforts to unveil the mechanism and ultimate toxin responsible for alcohol-induced cardiac toxicity, neither has been clarified thus far. Primary candidates for the specific toxins are ethanol, its first and major metabolic product - acetaldehyde (ACA) and fatty acid ethyl esters. Evidence from our lab suggests that ACA directly impairs cardiac function and promotes lipid peroxidation resulting in oxidative damage. The ACA-induced cardiac contractile depression may be reconciled with inhibitors of Cytochrome P-450 oxidase, xanthine oxidase and lipid peroxidation Unfortunately, the common methods to investigate the toxicity of ACA have been hampered by the fact that direct intake of ACA is toxic and unsuitable for chronic study, which is unable to provide direct evidence of direct cardiac toxicity for ACA. In order to overcome this obstacle associated with the chemical properties of ACA, our laboratory has used the chronic ethanol feeding model in transgenic mice with cardiac over-expression of alcohol dehydrogenase (ADH) and an in vitro ventricular myocyte culture model. The combination of both in vivo and in vitro approaches allows us to evaluate the role of ACA in ethanol-induced cardiac toxicity and certain cellular signaling pathways leading to alcoholic cardiomyopathy

The rate of polymyalgia rheumatica (PMR) and remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome in a clinic where primary care physicians are working in Japan

We analyzed the rate of polymyalgia rheumatica (PMR) and remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome, both characterized as seronegative inflammatory arthritis in elderly, in an outpatient unit where primary care physicians are working in Japan to better understand the epidemiological characteristics of the diseases in Japan. Consecutive outpatients who newly visited at Department of General Medicine, Asahikawa Medical University Hospital, Japan, between April 2004 and March 2010 were analyzed. Each parameter such as age, sex, diagnosis, and biochemical examination was investigated. During the 6 years, 10 or 3 patients were diagnosed as PMR or RS3PE syndrome, respectively. The patients with PMR were 7 women and 3 men, and the average age at diagnosis was 69. Out of all patients aged over 50 (n = 3,347), the rate of PMR was 0.22% in men or 0.36% in women, respectively. On the other hand, RS3PE syndrome was diagnosed in 3 men (76, 76, and 81 years old). The rate of patients with RS3PE syndrome was 0.09% among outpatients aged over 50 indicating that the rate of PMR in an outpatient clinic in Japan is not far from previous findings reported from western countries. When compared with PMR, the rate of RS3PE syndrome was approximately one-third, providing for the first time the rate of RS3PE syndrome when compared with PMR. These epidemilogical data might help us pick up the diseases in primary care setting in Japan

Dibutyltin Disrupts Glucocorticoid Receptor Function and Impairs Glucocorticoid-Induced Suppression of Cytokine Production

BACKGROUND: Organotins are highly toxic and widely distributed environmental chemicals. Dibutyltin (DBT) is used as stabilizer in the production of polyvinyl chloride plastics, and it is also the major metabolite formed from tributyltin (TBT) in vivo. DBT is immunotoxic, however, the responsible targets remain to be defined. Due to the importance of glucocorticoids in immune-modulation, we investigated whether DBT could interfere with glucocorticoid receptor (GR) function. METHODOLOGY: We used HEK-293 cells transiently transfected with human GR as well as rat H4IIE hepatoma cells and native human macrophages and human THP-1 macrophages expressing endogenous receptor to study organotin effects on GR function. Docking of organotins was used to investigate the binding mechanism. PRINCIPAL FINDINGS: We found that nanomolar concentrations of DBT, but not other organotins tested, inhibit ligand binding to GR and its transcriptional activity. Docking analysis indicated that DBT inhibits GR activation allosterically by inserting into a site close to the steroid-binding pocket, which disrupts a key interaction between the A-ring of the glucocorticoid and the GR. DBT inhibited glucocorticoid-induced expression of phosphoenolpyruvate carboxykinase (PEPCK) and tyrosine-aminotransferase (TAT) and abolished the glucocorticoid-mediated transrepression of TNF-alpha-induced NF-kappaB activity. Moreover, DBT abrogated the glucocorticoid-mediated suppression of interleukin-6 (IL-6) and TNF-alpha production in lipopolysaccharide (LPS)-stimulated native human macrophages and human THP-1 macrophages. CONCLUSIONS: DBT inhibits ligand binding to GR and subsequent activation of the receptor. By blocking GR activation, DBT may disturb metabolic functions and modulation of the immune system, providing an explanation for some of the toxic effects of this organotin

A Jak2 inhibitor, AG490, reverses lipin-1 suppression by TNF-α in 3T3-L1 adipocytes

http://dx.doi.org/10.1016/j.bbrc.2009.03.021Lipin-1 is a multifunctional metabolic regulator, involving in triacylglycerol and bioactive glycerolipids synthesis as an enzyme, transcriptional regulation as a coactivator, and adipogenesis. In obesity, adipose lipin-1 expression is decreased. Although lipin-1 is implicated in the pathogenesis of obesity, the mechanism is still not clear. Since TNF-α is deeply involved in the pathogenesis of obesity, insulin resistance, and diabetes, here we investigated the role of TNF-α on lipin-1 expression in adipocytes. Quantitative PCR studies showed that TNF-α suppressed both lipin-1A and -1B isoform expression in time- and dose-dependent manners in mature 3T3-L1 adpocytes. A Jak2 inhibitor, AG490, reversed the suppressive effect of TNF-α on both lipin-1A and -1B. In contrast, NF-κB, MAPKs, ceramide, and β-catenin pathway tested were not involved in the mechanism. These results suggest that TNF-α could be involved in obesity-induced lipin-1 suppression in adipocytes and Jak2 may play an important role in the mechanism