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Network interference, where the outcome of an individual is affected by the treatment assignment of those in their social network, is pervasive in real-world settings. However, it poses a challenge to estimating causal effects. We consider the task of estimating the total treatment effect (TTE), or the difference between the average outcomes of the population when everyone is treated versus when no one is, under network interference. Under a Bernoulli randomized design, we provide an unbiased estimator for the TTE when network interference effects are constrained to low-order interactions among neighbors of an individual. We make no assumptions on the graph other than bounded degree, allowing for well-connected networks that may not be easily clustered. We derive a bound on the variance of our estimator and show in simulated experiments that it performs well compared with standard estimators for the TTE. We also derive a minimax lower bound on the mean squared error of our estimator, which suggests that the difficulty of estimation can be characterized by the degree of interactions in the potential outcomes model. We also prove that our estimator is asymptotically normal under boundedness conditions on the network degree and potential outcomes model. Central to our contribution is a new framework for balancing model flexibility and statistical complexity as captured by this low-order interactions structure.

Determining the spatial patterning of tree species can provide inferences on underlying ecological processes. Gonystylus brunnescens is a South-east Asian subcanopy forest tree. To determine the spatial patterns of this species, we recorded the distribution of all individuals in a 0.4 ha sampling plot in eastern Borneo. We found that the pattern deviated from random and was well-described by the Matérn cluster model; clusters had a radius of approximately 4.2 m and contained an average of six seedlings each. This supports the hypothesis of animal-dispersed seeds and, due to a clear lack of association of juveniles with adults, may be due to scatter-hoarding of seeds by small mammal seed dispersers.

Ho3+:YAG amplifiers are able to efficiently scale pulse energy at wavelengths far shorter than the main emission peak. For 24 W input power at 2048 nm a signal output power of 81.6 W is reached, resulting in 5.3 dB gain.

Developing a device to retrieve the full Stokes’ vector at high-speed requires a careful design. We present an analysis of the measurement error of a polarimeter as a function of all optical component defects.

Tyrosine kinase inhibitors (TKI) have improved prognosis in metastatic anaplastic lymphoma kinase (ALK)‐driven lung adenocarcinoma, but patient outcomes vary widely. We retrospectively analyzed the clinical course of all cases with assessable baseline TP53 status and/or ALK fusion variant treated at our institutions (n = 102). TP53 mutations were present in 17/87 (20%) and the echinoderm microtubule‐associated protein‐like 4 (EML4)‐ALK variant 3 (V3) in 41/92 (45%) patients. The number of metastatic sites at diagnosis was affected more by the presence of V3 than by TP53 mutations, and highest with both factors (mean 5.3, p < 0.001). Under treatment with ALK TKI, progression‐free survival (PFS) was shorter with either TP53 mutations or V3, while double positive cases appeared to have an even higher risk (hazard ratio [HR] = 2.9, p = 0.015). The negative effect of V3 on PFS of TKI‐treated patients was strong already in the first line (HR = 2.5, p = 0.037) and decreased subsequently, whereas a trend for PFS impairment under first‐line TKI by TP53 mutations became stronger and statistically significant only when considering all treatment lines together. Overall survival was impaired more by TP53 mutations (HR = 4.9, p = 0.003) than by V3 (HR = 2.4, p = 0.018), while patients with TP53 mutated V3‐driven tumors carried the highest risk of death (HR = 9.1, p = 0.02). Thus, TP53 mutations and V3 are independently associated with enhanced metastatic spread, shorter TKI responses and inferior overall survival in ALK+ lung adenocarcinoma. Both markers could assist selection of cases for more aggressive management and guide development of novel therapeutic strategies. In combination, they define a patient subset with very poor outcome. What's new? This is the first study on the clinical impact of TP53 mutations in ALK‐driven lung adenocarcinoma that simultaneously considers the adverse effects of EML4‐ALK fusion variant 3. Both molecular features are independently associated with more aggressive disease course, including metastases to more organs, shorter responses to tyrosine kinase inhibitors, and worse overall survival. Their effects appear to be synergistic, and double‐positive cases have a very poor outcome. Both markers could assist patient selection for more aggressive management and help develop novel therapeutic strategies. [ABSTRACT FROM AUTHOR]