2,554 research outputs found
Threshold effects as the origin of , and observed in
We investigate the decay via various rescattering
diagrams. Without introducing genuine exotic resonances, it is shown that the
, and reported by the LHCb collaboration
can be simulated by the , and threshold cusps, respectively. These cusps are enhanced by some nearby
triangle singularities. The with cannot be well simulated
by the threshold effects in our model, which implies that it may be a genuine
resonance.Comment: 7 pages, 6 figures, 2 table
1-[4-(2-Chloroethoxy)-2-hydroxyphenyl]ethanone
In the title compound, C10H11ClO3, obtained by the reaction of 2,4-dihydroxyacetophenone, potassium carbonate and 1-bromo-2-chloroethane, an intramolecular O—H⋯O hydrogen bond occurs
Preparation of total flavonoids from loquat flower and its protective effect on acute alcohol-induced liver injury in mice
AbstractThis study aimed to research the preparation techniques of total flavones from loquat flower (TFLF), its anti-oxidation capacity, and its protective effect on hepatic injury. The best extraction parameters by orthogonal experimentation were water at 100°C, extraction time 2.5 hours, solid/liquid ratio 1:20, and three decoctions. The chromogenic reaction to the flavones showed that loquat flowers mainly contained flavone, flavonol, and flavanone compounds combining ortho-phenolic hydroxyl group structure in the 10–30% ethanol fraction. The anti-oxidant capacity of O2−· was 26.09% and of OH−·was 83.01% by salicylic acid and pyrogallol auto-oxidation. Compared with the model group, TFLF lowered the levels of alanine aminotransferase, aspartate aminotransferase, triglyceride, and malondialdehyde and liver index significantly, and upregulated the expression of adipose triglyceride lipase and Heine oxygenase-1 mRNA. The present findings suggest that TFLF has protective effect on acute alcoholinduced liver injury in mice and may be related to its antioxidant and free-radical scavenging activity
Myofascial trigger points: spontaneous electrical activity and its consequences for pain induction and propagation
Active myofascial trigger points are one of the major peripheral pain generators for regional and generalized musculoskeletal pain conditions. Myofascial trigger points are also the targets for acupuncture and/or dry needling therapies. Recent evidence in the understanding of the pathophysiology of myofascial trigger points supports The Integrated Hypothesis for the trigger point formation; however unanswered questions remain. Current evidence shows that spontaneous electrical activity at myofascial trigger point originates from the extrafusal motor endplate. The spontaneous electrical activity represents focal muscle fiber contraction and/or muscle cramp potentials depending on trigger point sensitivity. Local pain and tenderness at myofascial trigger points are largely due to nociceptor sensitization with a lesser contribution from non-nociceptor sensitization. Nociceptor and non-nociceptor sensitization at myofascial trigger points may be part of the process of muscle ischemia associated with sustained focal muscle contraction and/or muscle cramps. Referred pain is dependent on the sensitivity of myofascial trigger points. Active myofascial trigger points may play an important role in the transition from localized pain to generalized pain conditions via the enhanced central sensitization, decreased descending inhibition and dysfunctional motor control strategy
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