34 research outputs found

    Can A Pseudo-Nambu-Goldstone Higgs Lead To Symmetry Non-Restoration?

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    The calculation of finite temperature contributions to the scalar potential in a quantum field theory is similar to the calculation of loop corrections at zero temperature. In natural extensions of the Standard Model where loop corrections to the Higgs potential cancel between Standard Model degrees of freedom and their symmetry partners, it is interesting to contemplate whether finite temperature corrections also cancel, raising the question of whether a broken phase of electroweak symmetry may persist at high temperature. It is well known that this does not happen in supersymmetric theories because the thermal contributions of bosons and fermions do not cancel each other. However, for theories with same spin partners, the answer is less obvious. Using the Twin Higgs model as a benchmark, we show that although thermal corrections do cancel at the level of quadratic divergences, subleading corrections still drive the system to a restored phase. We further argue that our conclusions generalize to other well-known extensions of the Standard Model where the Higgs is rendered natural by being the pseudo-Nambu-Goldstone mode of an approximate global symmetry.Comment: 21 pages, 5 figures. v2: fixed problem related to references with 9-digit arXiv identifiers. v3: references added v4: Some clarifications and more references added; matches published versio

    Fast exploration and learning of latent graphs with aliased observations

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    We consider the problem of recovering a latent graph where the observations at each node are \emph{aliased}, and transitions are stochastic. Observations are gathered by an agent traversing the graph. Aliasing means that multiple nodes emit the same observation, so the agent can not know in which node it is located. The agent needs to uncover the hidden topology as accurately as possible and in as few steps as possible. This is equivalent to efficient recovery of the transition probabilities of a partially observable Markov decision process (POMDP) in which the observation probabilities are known. An algorithm for efficiently exploring (and ultimately recovering) the latent graph is provided. Our approach is exponentially faster than naive exploration in a variety of challenging topologies with aliased observations while remaining competitive with existing baselines in the unaliased regime

    Schema-learning and rebinding as mechanisms of in-context learning and emergence

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    In-context learning (ICL) is one of the most powerful and most unexpected capabilities to emerge in recent transformer-based large language models (LLMs). Yet the mechanisms that underlie it are poorly understood. In this paper, we demonstrate that comparable ICL capabilities can be acquired by an alternative sequence prediction learning method using clone-structured causal graphs (CSCGs). Moreover, a key property of CSCGs is that, unlike transformer-based LLMs, they are {\em interpretable}, which considerably simplifies the task of explaining how ICL works. Specifically, we show that it uses a combination of (a) learning template (schema) circuits for pattern completion, (b) retrieving relevant templates in a context-sensitive manner, and (c) rebinding of novel tokens to appropriate slots in the templates. We go on to marshall evidence for the hypothesis that similar mechanisms underlie ICL in LLMs. For example, we find that, with CSCGs as with LLMs, different capabilities emerge at different levels of overparameterization, suggesting that overparameterization helps in learning more complex template (schema) circuits. By showing how ICL can be achieved with small models and datasets, we open up a path to novel architectures, and take a vital step towards a more general understanding of the mechanics behind this important capability

    Acquired rifampicin resistance in thrice-weekly antituberculosis therapy: impact of HIV and antiretroviral therapy

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    Risk factors for acquired rifampicin resistance (ARR) among tuberculosis patients on thrice-weekly antituberculosis therapy were baseline isoniazid resistance and HIV. Among HIV-infected patients, higher mycobacterial burden and lower CD4 count, but not highly active antiretroviral therapy, were significantly associated with ARR. Background: Risk factors for acquired rifampicin resistance (ARR) in human immunodeficiency virus (HIV)/tuberculosis coinfection, in the highly active antiretroviral therapy (HAART) era, needs evaluation. We studied the impact of HIV and HAART on ARR among patients taking thrice-weekly antituberculosis therapy. Methods: This cross-protocol analysis included patients with newly diagnosed, rifampicin-susceptible pulmonary tuberculosis, with and without HIV, enrolled in clinical trials (who took >80% of medication) at the National Institute for Research in Tuberculosis between 1999 and 2013. All patients received rifampicin and isoniazid for 6 months reinforced with pyrazinamide and ethambutol in the first 2 months, given thrice-weekly throughout the study along with HAART in one of the groups. Outcomes were categorized and multivariate logistic regression analysis performed to identify risk factors for ARR. Results: The per-protocol results included patients with tuberculosis: 246 HIV-uninfected patients (HIV–TB+), 212 HIV patients not on HAART (non-HAART), and 116 HIV-infected patients on HAART. Median CD4 counts of the latter 2 groups were 150 and 93 cells/μL, respectively, and the median viral loads were 147 000 and 266 000 copies/mL, respectively. Compared with HIV–TB+, the relative risks (RRs) for an unfavorable response in the coinfected, non-HAART and HAART groups were 2.1 (95% confidence interval [CI], 1.7–14.8; P<.0001) and 2.1 (95% CI, .9–5.2; P=.3), whereas for ARR, the RRs were 21.1 (95% CI, 2.6–184; P<.001) and 8.2 (95% CI, .6–104; P=.07), respectively. Conclusions: HIV-infected patients with tuberculosis treated with a thrice-weekly antituberculosis regimen are at a higher risk of ARR, compared with HIV-uninfected patients, in the presence of baseline isoniazid resistance. HAART reduces but does not eliminate the risk of ARR
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