2,359 research outputs found

    Relationship of Cellular Adhesion Molecules and Stress Hormones in Obese Males Following Exercise

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    The development of atherosclerosis is associated with a steady accumulation of inflammatory molecules. Exercise-induced hormones such as cortisol and catecholamines (epinephrine and norepinephrine) may play a role in endothelial inflammation. Methods: Fifteen obese (BMI \u3e 30 kg/m2) sedentary (less than 2 days per week of physical activity) male volunteers, the ages between 18 and30, participated in the study. The participants performed a single bout of cycling exercise (average energy expenditure ~ 300 kcal) at two different intensities in random order [low-intensity: 50% of maximal heart rate and high-intensity: 80% of maximal heart rate]. Overnight fasting blood samples were collected at baseline, immediate post-exercise (IPE), 1-hr PE, and 24-hr PE for each intensity of exercise to determine the responses of soluble cell adhesion molecules [intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), and E-selectin (sE-selectin)] and exercise-induced stress hormones. Data were analyzed by an analysis of variance with repeated measures along with the Bonferroni multiple comparisons. The linear regression analysis was used to examine the interaction between exercise-induced hormones and vascular inflammation markers (p \u3c .05). RESULTS: There exhibited no significant change in sICAM-1, sVCAM-1, E or NE, while sE-selectin at 1-hr PE (10.25±1.07 ng/mL) significantly decreased (p = .045) from baseline (12.22±1.39 ng/mL). COR at IPE (262.12±31.09 ng/ml) was significantly higher (p = .001) than 1-hr PE (189.35±31.11 ng/ml) during high-intensity exercise. In contrast, COR at IPE (187.52±31.09 ng/ml, p = .009) and 1-hr PE (156.24±31.11 ng/ml, p = .001) were significantly lower than baseline (259.75±23.07 ng/ml) during low-intensity exercise. COR and sICAM-1 had a negative relationship at 1-hr PE during low-intensity exercise (r2 = .34, p = .02), whereas COR and sVCAM-1 had a positive relationship at IPE during high-intensity exercise (r2 = .36, p = .02). CONCLUSION: sE-selectin was favorably reduced following exercise, and changes in cortisol were exercise-intensity dependent. Although sICAM-1 and sVCAM-1 did not significantly change following exercise, a significant interaction between cortisol and these cell adhesion molecules suggests that cortisol is one of the responsible exercise-induced hormones that may be associated with cell adhesion molecule metabolism

    Lymphocyte apoptosis, macrophage function and disease activity in systemic lupus erythematosus (SLE)

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    INTRODUCTION: Increased lymphocyte apoptosis and defects in macrophage removal of apoptotic cells have been suggested to contribute to the development of SLE. The aim of this study was to investigate the relationship between peripheral lymphocyte apoptosis, macrophage function as determined by the serum levels of neopterin …published_or_final_versio

    LAPTM4B Targeting as Potential Therapy for Hepatocellular Carcinoma

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    HCC is one of the most common cancers worldwide with high prevalence, recurrence, and lethality. The curative rate is not satisfactory. LAPTM4B is a novel driver gene of HCC first indentified by our group. It is over-expressed in 87.3% of HCC. The expression levels of the encoded LAPTM4B-35 protein in HCC is also over-expressed in 86.2% of HCC and shows a significant positive correlation with pathological grade, metastasis, and recurrence, and a negative correlation with postoperative overall- and cancer free- survival of HCC patients. Moreover, HCC cells showing high expression of LAPTM4B-35 show a strong tendency to metastasize and enhanced drug resistance. Overexpression of this gene promotes tumorigenesis, faster growth of human HCC xenografts and metastasis in nude mice, and leads to anti-apoptosis, deregulation of proliferation, enhancement of migration and invasion, as well as multi-drug resistance. In addition, overexpression of LAPTM4B-35 leads to accumulation of a number of oncoproteins and to down-regulation of a number of tumor suppressing proteins. By contrary, knockdown of endogenous LAPTM4B-35 via RNAi results in remarkable inhibition of xenograft growth and metastasis of human HCC in nude mice. Also, RNAi knockdown of LAPTN4B-35 can reverse the cellular and molecular malignant phenotypes noted above

    Protective spin-labeled fluorenes maintain amyloid beta peptide in small oligomers and limit transitions in secondary structure

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    Alzheimer’s disease is characterized by the presence of extracellular plaques comprised of amyloid beta (Aβ) peptides. Soluble oligomers of the Aβ peptide underlie a cascade of neuronal loss and dysfunction associated with Alzheimer's disease. Single particle analyses of Aβ oligomers in solution by fluorescence correlation spectroscopy (FCS) were used to provide real-time descriptions of how spin-labeled fluorenes (SLFs; bi-functional small molecules that block the toxicity of Aβ) prevent and disrupt oligomeric assemblies of Aβ in solution. Furthermore, the circular dichroism (CD) spectrum of untreated Aβ shows a continuous, progressive change over a 24-hour period, while the spectrum of Aβ treated with SLF remains relatively constant following initial incubation. These findings suggest the conformation of Aβ within the oligomer provides a complementary determinant of Aβ toxicity in addition to oligomer growth and size. Although SLF does not produce a dominant state of secondary structure in Aβ, it does induce a net reduction in beta secondary content compared to untreated samples of Aβ. The FCS results, combined with electron paramagnetic resonance spectroscopy and CD spectroscopy, demonstrate SLFs can inhibit the growth of Aβ oligomers and disrupt existing oligomers, while retaining Aβ as a population of smaller, yet largely disordered oligomers

    Validation of handheld fundus camera with mydriasis for retinal imaging of diabetic retinopathy screening in China: a prospective comparison study.

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    OBJECTIVES: To investigate the clinical validity of using a handheld fundus camera to detect diabetic retinopathy (DR) in China. DESIGN AND SETTINGS: Prospective comparison study of the handheld fundus camera with a standard validated instrument in detection of DR in hospital and a community screening clinic in Guangdong Province, China. PARTICIPANTS: Participants aged 18 years and over with diabetes who were able to provide informed consent and agreed to attend the dilated eye examination with handheld tests and a standard desktop camera. PRIMARY AND SECONDARY OUTCOME MEASURES: Primary outcome was the proportion of those with referable DR (R2 and above) identified by the handheld fundus camera (the index test) compared with the standard camera. Secondary outcome was the comparison of proportion of gradable images obtained from each test. RESULTS: In this study, we examined 304 people (608 eyes) with each of the two cameras under mydriasis. The handheld camera detected 119 eyes (19.5%) with some level of DR, 81 (13.3%) of them were referable, while the standard camera detected 132 eyes (21.7%) with some level of DR and 83 (13.7%) were referable. It seems that the standard camera found more eyes with referable DR, although McNemar's test detected no significant difference between the two cameras.Of the 608 eyes with images obtained by desktop camera, 598 (98.4%) images were of sufficient quality for grading, 12 (1.9%) images were not gradable. By the handheld camera, 590 (97.0%) were gradable and 20 (3.2%) images were not gradable.The two cameras reached high agreement on diagnosis of retinopathy and maculopathy at all the levels of retinopathy. CONCLUSION: Although it could not take the place of standard desktop camera on clinic fundus examination, the handheld fundus camera showed promising role on preliminary DR screening at primary level in China. To ensure quality images, mydriasis is required

    Responses of Matrix Metalloproteinases in Obese Men after Undergoing Low and High Intensity Exercise

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    Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases that degrade extracellular matrix proteins and play a role in various pathological conditions such as inflammation and endothelial dysfunction. PURPOSE: The current study investigated the responses of MMP-1, -2, and -9 in obese men over a 24-hour period after undergoing different intensities (low vs. high) of cycling exercise. METHODS: Fifteen sedentary (physical activity \u3c 2 days/week) obese [body mass index (BMI) \u3e 30kg/m2] men between the ages of 18 and 30 years participated in the study. Each participant completed a similar volume (average energy expenditure ~ 300 kcal) of cycling exercise at 2 different intensities in random order [low intensity: 50% of maximal heart rate and high-intensity: 80% of maximal heart rate] on a separate occasion. Fasting overnight blood samples were collected at baseline, immediate post exercise (IPE), 1-hour post exercise (1-PE), and 24-hours post exercise (24-PE) for each exercise intensity trial to examine the responses of MMP-1, -2, and -9. An analysis of variance (ANOVA) with repeated measures was used to determine the mean differences in intensity and time on MMP-1, -2, and -9. If necessary, the Sidak’s multiple pairwise comparisons and a follow-up Simple effects test were employed as a post-hot test (p \u3c 0.05). RESULTS: No change was found in MMP-1 following either low- or high-intensity exercise over the 24-hr period. During the low-intensity exercise trial, MMP-2 at 24-hr PE (72.68±6.43 ng/mL) was significantly lower than IPE (87.23±8.02 ng/mL, p=0.008) and 1-hr PE (92.01±7.99 ng/mL, p=0.011). During the high-intensity exercise trial, MMP-9 at IPE (54.19±9.16 ng/mL) was significantly higher than PRE (30.48±5.86 ng/mL, p =0.008), 1-hr PE (34.82±5.08 ng/mL, p=0.040), and 24-hr PE (31.03±4.82 ng/mL, p=0.006). Additionally, MMP-9 at 24-hr PE (31.32±4.82 ng/mL) was significantly lower than PRE (41.43±5.86 ng/mL, p=0.009) during the low-intensity exercise trial. CONCLUSION: Both MMP-2 and -9, but not MMP-1, significantly increased immediately following exercise, which then returned to its baseline values post exercise. This exercise-induced acute change in MMP-2 and MMP-9 was dependent upon exercise intensity since MMP-2 changed with low-intensity exercise, whereas MMP-9 was altered following high-intensity exercise. Additionally, MMP-9 at 24 hours decreased after 24 hours following low intensity exercise. Thus, the current study suggests that the responses of MMP-2 and MMP-9 to exercise are dependent on exercise-intensity, and low-intensity exercise may favorably influence cardiovascular health by lowering both MMP-2 and MMP-9 in obese men

    Resonances in J/ψ→ϕπ+π−J/\psi \to \phi \pi ^+\pi ^- and ϕK+K−\phi K^+K^-

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    A partial wave analysis is presented of J/ψ→ϕπ+π−J/\psi \to \phi \pi ^+\pi ^- and ϕK+K−\phi K^+K^- from a sample of 58M J/ψJ/\psi events in the BES II detector. The f0(980)f_0(980) is observed clearly in both sets of data, and parameters of the Flatt\' e formula are determined accurately: M=965±8M = 965 \pm 8 (stat) ±6\pm 6 (syst) MeV/c2^2, g1=165±10±15g_1 = 165 \pm 10 \pm 15 MeV/c2^2, g2/g1=4.21±0.25±0.21g_2/g_1 = 4.21 \pm 0.25 \pm 0.21. The ϕππ\phi \pi \pi data also exhibit a strong ππ\pi \pi peak centred at M=1335M = 1335 MeV/c2^2. It may be fitted with f2(1270)f_2(1270) and a dominant 0+0^+ signal made from f0(1370)f_0(1370) interfering with a smaller f0(1500)f_0(1500) component. There is evidence that the f0(1370)f_0(1370) signal is resonant, from interference with f2(1270)f_2(1270). There is also a state in ππ\pi \pi with M=1790−30+40M = 1790 ^{+40}_{-30} MeV/c2^2 and Γ=270−30+60\Gamma = 270 ^{+60}_{-30} MeV/c2^2; spin 0 is preferred over spin 2. This state, f0(1790)f_0(1790), is distinct from f0(1710)f_0(1710). The ϕKKˉ\phi K\bar K data contain a strong peak due to f2′(1525)f_2'(1525). A shoulder on its upper side may be fitted by interference between f0(1500)f_0(1500) and f0(1710)f_0(1710).Comment: 17 pages, 6 figures, 1 table. Submitted to Phys. Lett.

    First Measurements of eta_c Decaying into K^+K^-2(pi^+pi^-) and 3(pi^+pi^-)

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    The decays of eta_c to K^+K^-2(pi^+pi^-) and 3(pi^+pi^-) are observed for the first time using a sample of 5.8X10^7 J/\psi events collected by the BESII detector. The product branching fractions are determined to be B(J/\psi-->gamma eta_c)*B(eta_c-->K^+K^-pi^+pi^-pi^+pi^-)=(1.21+-0.32+- 0.23)X10^{-4},B(J/ψ−−>gammaetac)∗B(etac−−>K∗0Kˉ∗0pi+pi−)=(1.29+−0.43+−0.32)X10−4,B(J/\psi-->gamma eta_c)*B(eta_c-->K^{*0}\bar{K}^{*0}pi^+pi^-)= (1.29+-0.43+-0.32)X10^{-4}, and (J/\psi-->gamma eta_c)* B(eta_c-->pi^+pi^-pi^+pi^-pi^+pi^-)= (2.59+-0.32+-0.48)X10^{-4}. The upper limit for eta_c-->phi pi^+pi^-pi^+pi^- is also obtained as B(J/\psi-->gamma eta_c)*B(eta_c--> phi pi^+pi^-pi^+pi^-)< 6.03 X10^{-5} at the 90% confidence level.Comment: 11 pages, 4 figure

    Measurement of the Branching Fraction of J/psi --> pi+ pi- pi0

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    Using 58 million J/psi and 14 million psi' decays obtained by the BESII experiment, the branching fraction of J/psi --> pi+ pi- pi0 is determined. The result is (2.10+/-0.12)X10^{-2}, which is significantly higher than previous measurements.Comment: 9 pages, 8 figures, RevTex
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