| 1. |
- Ablikim, M., et al.
(författare)
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Amplitude analysis of the pi(0)pi(0) system produced in radiative J/psi decays
- 2015
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Ingår i: Physical Review D. - 1550-7998 .- 1550-2368. ; 92:5
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Tidskriftsartikel (refereegranskat)abstract
- An amplitude analysis of the pi(0)pi(0) system produced in radiative J/psi decays is presented. In particular, a piecewise function that describes the dynamics of the pi(0)pi(0) system is determined as a function of M pi(0)pi(0) from an analysis of the (1.311 +/- 0.011) x 10(9) J/psi decays collected by the BESIII detector. The goal of this analysis is to provide a description of the scalar and tensor components of the pi(0)pi(0) system while making minimal assumptions about the properties or number of poles in the amplitude. Such a model-independent description allows one to integrate these results with other related results from complementary reactions in the development of phenomenological models, which can then be used to directly fit experimental data to obtain parameters of interest. The branching fraction of J/psi -> pi(0)pi(0) is determined to be (1.15 +/- 0.05) x 10(-3), where the uncertainty is systematic only and the statistical uncertainty is negligible.
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| 2. |
- Jackura, A., et al.
(författare)
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New analysis of eta pi tensor resonances measured at the COMPASS experiment
- 2018
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Ingår i: Physics Letters B. - : Elsevier BV. - 0370-2693 .- 1873-2445. ; 779, s. 464-472
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Tidskriftsartikel (refereegranskat)abstract
- We present a new amplitude analysis of the eta pi D-wave in the reaction pi(-) p -> eta pi(-) p measured by COMPASS. Employing an analytical model based on the principles of the relativistic S-matrix, we find two resonances that can be identified with the a(2)(1320) and the excited a(2)(1700), and perform a comprehensive analysis of their pole positions. For the mass and width of the a(2) we find M = (1307 +/- 1 6) MeV and Gamma=(112 +/- 1 +/- 8) MeV, and for the excited state a(2)' we obtain M = (1720 +/- 10 +/- 60) MeV and Gamma = (280 +/- 10 +/- 70) MeV, respectively.
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| 3. |
- Skiba, DS, et al.
(författare)
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Hypertensive Effect of Downregulation of the Opioid System in Mouse Model of Different Activity of the Endogenous Opioid System
- 2021
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Ingår i: International journal of molecular sciences. - : MDPI AG. - 1422-0067. ; 22:8
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Tidskriftsartikel (refereegranskat)abstract
- The opioid system is well-known for its role in modulating nociception and addiction development. However, there are premises that the endogenous opioid system may also affect blood pressure. The main goal of the present study was to determine the impact of different endogenous opioid system activity and its pharmacological blockade on blood pressure. Moreover, we examined the vascular function in hyper- and hypoactive states of the opioid system and its pharmacological modification. In our study, we used two mouse lines which are divergently bred for high (HA) and low (LA) swim stress-induced analgesia. The obtained results indicated that individuals with low endogenous opioid system activity have higher basal blood pressure compared to those with a hyperactive opioid system. Additionally, naloxone administration only resulted in the elevation of blood pressure in HA mice. We also showed that the hypoactive opioid system contributes to impaired vascular relaxation independent of endothelium, which corresponded with decreased guanylyl cyclase levels in the aorta. Together, these data suggest that higher basal blood pressure in LA mice is a result of disturbed mechanisms in vascular relaxation in smooth muscle cells. We believe that a novel mechanism which involves endogenous opioid system activity in the regulation of blood pressure will be a promising target for further studies in hypertension development.
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| 4. |
- Mohanta, S. K., et al.
(författare)
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Neuroimmune cardiovascular interfaces control atherosclerosis
- 2022
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 605, s. 152-159
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Tidskriftsartikel (refereegranskat)abstract
- Atherosclerotic plaques develop in the inner intimal layer of arteries and can cause heart attacks and strokes(1). As plaques lack innervation, the effects of neuronal control on atherosclerosis remain unclear. However, the immune system respondsto plaques by forming leukocyte infiltrates in the outer connective tissue coat of arteries (the adventitia)(2-6). Here, because the peripheral nervous system uses the adventitia as its principal conduit to reach distant targets(7-9), we postulated that the peripheral nervous system may directly interact with diseased arteries. Unexpectedly, widespread neuroimmune cardiovascular interfaces (NICIs) arose in mouse and human atherosclerosis-diseased adventitia segments showed expanded axon networks, includinggrowth cones at axon endings near immune cells and media smooth muscle cells. Mouse NICIs established a structural artery-brain circuit (ABC): abdominal adventitia nociceptive afferents(10-14) entered the central nervous system through spinal cord T-6-T-13 dorsal root ganglia and were traced to higher brain regions, including the parabrachial and central amygdala neurons; and sympathetic efferent neurons projected from medullary and hypothalamic neuronsto the adventitia through spinal intermediolateral neurons and both coeliac and sympathetic chain ganglia. Moreover, ABC peripheral nervous system components were activated: splenic sympathetic and coeliac vagus nerve activities increased in parallel to disease progression, whereas coeliacganglionectomy led to the disintegration of adventitial NICIs, reduced disease progression and enhanced plaque stability. Thus, the peripheral nervous system uses NICIs to assemble a structural ABC, and therapeutic intervention in the ABC attenuates atherosclerosis.
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