191 research outputs found
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
Characteristics in patients with headache in an outpatient clinic in Japan
<p>Abstract</p> <p>Background</p> <p>Little is known about the prevalence of primary and secondary headache in clinics in Japan. The aim of this study is to characterize patients with headache in an outpatient unit where primary care physicians are working in Japan.</p> <p>Methods</p> <p>Consecutive outpatients who newly visited the Department of General Medicine, Asahikawa Medical College Hospital, Asahikawa, Japan between April 2005 and March 2009 were analyzed. Each parameter such as age, sex or diagnosis was investigated.</p> <p>Results</p> <p>Out of 4693 patients, 418 patients visited to our department because of headache. Primary headache was found in 167 patients (39.9%). The rate of tension-type headache (TTH) (30.8%) was highest, followed by migraine (9.1%). Approximately 3 times higher rate of migraine was observed in female patients when compared with male patients. In female patients, migraine was observed more frequently in younger patients. On the other hands, TTH was observed in almost all aged patients in males and females, and the rate of TTH peaks between the ages of 40 and 49 years in both sex. The present study also demonstrated that 8.4% of patients who chiefly complained of headache had been diagnosed as depression while 1.7% of remained patients had been diagnosed as depression, indicating 5-times higher rate of depression in patients with headache.</p> <p>Conclusion</p> <p>All these results suggest that primary headache, especially TTH, is highly observed and depression should be considered in patients with headache in an outpatient clinic where primary care physicians are working in Japan.</p
Localization of an hTERT repressor region on human chromosome 3p21.3 using chromosome engineering
Telomerase is a ribonucleoprotein enzyme that synthesizes telomeric DNA. The reactivation of telomerase activity by aberrant upregulation/expression of its catalytic subunit hTERT is a major pathway in human tumorigenesis. However, regulatory mechanisms that control hTERT expression are largely unknown. Previously, we and others have demonstrated that the introduction of human chromosome 3, via microcell-mediated chromosome transfer (MMCT), repressed transcription of the hTERT gene. These results suggested that human chromosome 3 contains a regulatory factor(s) involved in the repression of hTERT. To further localize this putative hTERT repressor(s), we have developed a unique experimental approach by introducing various truncated chromosome 3 regions produced by a novel chromosomal engineering technology into the renal cell carcinoma cell line (RCC23 cells). These cells autonomously express ectopic hTERT (exohTERT) promoted by a retroviral LTR promoter in order to permit cellular division after repression of endogenous hTERT. We found a telomerase repressor region located within a 7-Mb interval on chromosome 3p21.3. These results provide important information regarding hTERT regulation and a unique method to identify hTERT repressor elements
Tributyltin (TBT) biodegradation induces oxidative stress of Cunninghamella echinulata
Tributyltin (TBT) is one of the most deleterious compounds introduced into natural environment by humans. The ability of Cunninghamella echinulata to degrade tributyltin (TBT) (5 mg l-1) as well as the effect of the xenobiotic on fungal amino acids composition and proteins profile were examined. C. echinulata removed 91% of the initial biocide concentration and formed less hazardous compounds dibutyltin (DBT) and monobutyltin (MBT). Moreover, the fungus produced a hydroxylated metabolite (TBTOH), in which the hydroxyl group was bound directly to the tin atom. Proteomics analysis showed that in the presence of TBT, the abundances of 22 protein bands were changed and the unique overexpressions of peroxiredoxin and nuclease enzymes were observed. Determination of free amino acids showed significant changes in the amounts of 19 from 23 detected metabolites. A parallel increase in the level of selected amino acids such as betaine, alanine, aminoisobutyrate or proline and peroxiredoxin enzyme in TBT-containing cultures revealed that TBT induced oxidative stress in the examined fungus.National Science Centre, Poland (Project No. UMO-2014/13/N/NZ9/00878)
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
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
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
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