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1.
Phys Rev Lett ; 131(5): 051601, 2023 Aug 04.
Artigo em Inglês | MEDLINE | ID: mdl-37595226

RESUMO

We find that the duality between color and kinematics can be used to inform the high energy behavior of effective field theories. Namely, we demonstrate that the massless gauge theory of Yang-Mills deformed by a higher-derivative F^{3} operator cannot be tree level color dual while consistently factorizing without a tower of additional four-point counterterms with rigidly fixed Wilson coefficients that reaches to the ultraviolet (UV). We find through explicit calculation a suggestive resummation, namely that their amplitudes are consistent with the α^{'} expansion of those generated by the (DF)^{2}+YM theory, a known color-dual theory where the F^{2} term has been given a mass squared proportional to 1/α^{'}. As a result, considering consistent double-copy construction as a physical principle implies that an F^{3}-based color-dual resolution of the UV divergence in N=4 supergravity comes at the cost of field-theoretic locality. Similarly, when double copying F^{3} with itself, double-copy consistency lifts R^{3} gravity to a family of gravity theories with an all-order tower of higher-derivative corrections, which includes the closed bosonic string as a standard adjoint-type double copy.

2.
Phys Rev Lett ; 123(25): 251103, 2019 Dec 20.
Artigo em Inglês | MEDLINE | ID: mdl-31922809

RESUMO

We derive new positivity bounds for scattering amplitudes in theories with a massless graviton in the spectrum in four spacetime dimensions, of relevance for the weak gravity conjecture and modified gravity theories. The bounds imply that extremal black holes are self-repulsive, M/|Q|<1 in suitable units, and that they are unstable to decay to smaller extremal black holes, providing an S-matrix proof of the weak gravity conjecture. We also present other applications of our bounds to the effective field theory of weakly broken Galileons, axions, and P(X) theories.

3.
J Neurophysiol ; 88(2): 699-714, 2002 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-12163523

RESUMO

Cisplatin causes both acute and chronic forms of tinnitus as well as increases in spontaneous neural activity (hyperactivity) in the dorsal cochlear nucleus (DCN) of hamsters. It has been hypothesized that the induction of hyperactivity in the DCN may be a consequence of cisplatin's effects on cochlear outer hair cells (OHCs); however, systematic studies testing this hypothesis have yet to appear in the literature. In the present investigation, the relationship between hyperactivity and OHC loss, induced by cisplatin, was examined in detail. Hamsters received five treatments of cisplatin at doses ranging from 1.5 to 3 mg. kg(-1). day(-1), every other day. Beginning 1 mo after initiation of treatment, electrophysiological recordings were carried out on the surface of the DCN to measure spontaneous multiunit activity along a set of coordinates spanning the medial-lateral (tonotopic) axis of the DCN. After recordings, cochleas were removed and studied histologically using a scanning electron microscope. The results revealed that cisplatin-treated animals with little or no loss of OHCs displayed levels of activity similar to those seen in saline-treated controls. In contrast, the majority (75%) of cisplatin-treated animals with severe OHC loss displayed well-developed hyperactivity in the DCN. The induced hyperactivity was seen mainly in the medial (high-frequency) half of the DCN of treated animals. This pattern was consistent with the observation that OHC loss was distributed mainly in the basal half of the cochlea. In several of the animals with severe OHC loss and hyperactivity, there was no significant damage to IHC stereocilia nor any observable irregularities of the reticular lamina that might have interfered with normal IHC function. Hyperactivity was also observed in the DCN of animals showing severe losses of OHCs accompanied by damage to IHCs, although the degree of hyperactivity in these animals was less than in animals with severe OHC loss but intact IHCs. These results support the view that loss of OHC function may be a trigger of tinnitus-related hyperactivity in the DCN and suggest that this hyperactivity may be somewhat offset by damage to IHCs.


Assuntos
Cisplatino/efeitos adversos , Núcleo Coclear/efeitos dos fármacos , Células Ciliadas Auditivas Externas/efeitos dos fármacos , Zumbido/induzido quimicamente , Potenciais de Ação/efeitos dos fármacos , Animais , Antineoplásicos/efeitos adversos , Morte Celular , Cóclea/cirurgia , Núcleo Coclear/fisiopatologia , Cricetinae , Eletrofisiologia , Células Ciliadas Auditivas Externas/fisiopatologia , Microscopia Eletrônica de Varredura , Zumbido/fisiopatologia
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