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The commonly used analytic bidirectional reflectance distribution functions (BRDFs) do not model goniochromatism, that is, angle-dependent material color. The material color is usually defined by a diffuse reflectance spectrum or RGB vector and a specular part based on a spectral complex index of refraction. Extension of the commonly used BRDFs based on wave theory can help model goniochromatism, but this comes at the cost of significant added model complexity. We measured the goniochromatism of structural color pigments used for additive color printing and found that we can fit the observed spectral angular dependence of the bidirectional reflectance using a simple modification of the standard microfacet BRDF model. All we need to describe the goniochromatism is an empirically based spectral parameter, which we use in our model together with a specular reflectance spectrum instead of the spectral complex index of refraction. We demonstrate the ability of our model to fit the measured reflectance of red, green, and blue commercial structural color pigments. Our BRDF model enables straightforward implementation of a shader for interactive preview of 3-D objects with printed spatially and angularly varying texture.

Introduction: Diagnostic error is a prevalent type of medical error that is associated with considerable patient harm and increased medical costs. The majority of literature guiding the current understanding of diagnostic error in the hospital setting is from adult studies. However, there is research to suggest this type of error is also prevalent in the pediatric specialty., Objectives: The primary objective of this study was to define the current understanding of diagnostic error in the pediatric hospital through a structured literature review., Methods: We searched PubMed and identified studies focusing on three aspects of diagnostic error in pediatric hospitals: the incidence or prevalence, contributing factors, and related interventions. We used a tiered review, and a standardized electronic form to extract data from included articles., Results: Fifty-nine abstracts were screened and 23 full-text studies were included in the final review. Seventeen of the 23 studies focused on the incidence or prevalence, with only 3 studies investigating the utility of interventions. Most studies took place in an intensive care unit or emergency department with very few studies including only patients on the general wards. Overall, the prevalence of diagnostic error in pediatric hospitals varied greatly and depended on the measurement technique and specific hospital setting. Both healthcare system factors and individual cognitive factors were found to contribute to diagnostic error, with there being limited evidence to guide how best to mitigate the influence of these factors on the diagnostic process., Conclusion: The general knowledge of diagnostic error in pediatric hospital settings is limited. Future work should incorporate structured frameworks to measure diagnostic errors and examine clinicians' diagnostic processes in real-time to help guide effective hospital-wide interventions.

Managing risk in cases that involve the use of clinical decision support tools is ethically complex. This article highlights some of these complexities and offers 3 considerations for risk managers to draw upon when assessing risk in cases using clinical decision support: (1) the type of decision support offered, (2) how well a decision support tool helps accomplish work that needs to be done, and (3) how well values embedded in a tool align with patients' and caregivers' professed values., (© 2020 American Medical Association. All Rights Reserved.)

The desensitizing potencies of angiotensin II (ANG II) analogues modified at positions 1, 2, 4, 7, and 8 have been examined in the rat isolated uterus assay by determining the time of recovery of the half-maximal concentration (EC50) response to angiotensin II after treatment of the tissues with a high dose (10(-5) M) of each analogue for 2 min. The magnitude of the desensitization effect was substituent dependent in the following manner: position 1, sarcosine (Sar) greater than Asp greater than des-Asp; position 2, Arg greater than Sar; position 4, Tyr greater than Tyr(Me) approximately Phe; position 7, 3,4-dehydroproline (Dpr) greater than Pro greater than thioproline (Tpr) greater than Sar; position 8, Ile greater than D-Trp greater than Ala greater than Phe. The "additivity" rule applied to these structure-desensitization relationships and the most potent desensitizer, requiring 3 h for reestablishment of the EC50 response, was [Sar1, Dpr7, Ile8]-ANG II. The desensitizing potencies of these analogues did not correlate with agonist or antagonist activities and demonstrated that the angiotensin-mediated tissue desensitization process has unique structural determinants. Methylation or elimination of the tyrosine hydroxyl group of strong desensitizers virtually eliminated the desensitization effect, implicating the phenoxyl moiety in the mechanism of desensitization. The initial phase of recovery of angiotensin responsiveness after desensitization by several analogues appeared to obey first-order kinetics. The results are discussed in the contexts of both one- and two-site receptor models.

Analogues of the type [1-sarcosine,7-sarcosine, 8-X]angiotensin II, where X = isoleucine, leucine, alanine, methionine, O-methylthreonine, or DL-alloisoleucine, were synthesized by the solid-phase method and purified by partition chromatography, cation-exchange chromatography, and high-pressure liquid chromatography. In the isolated rat uterus, these analogues had activities of less than 0.1, less than 0.1, less than 0.1, less than 0.1, less than 0.1, and 0.7%, respectively, of the hyotropic activity of angiotensin II and inhibited the contractile response to angiotensin II with pA2 values of 8.1, 7.2, 6.7, 7.7, 7.4, and 8.4, respectively. In the vagotomized ganglion blocked rat, the analogues had 0.7, 0.21, 0.06, 0.72, 0.13, and 12.5%, respectively, of the pressor activity of angiotensin II.

Rats exposed to technical grade dinitrotoluene (DNT) develop hepatocellular carcinomas. Humans may be exposed to DNT during its manufacture and use. To permit comparisons of human excretion patterns of DNT metabolites with those previously observed in rats, urine specimens were collected over a 72-hr period from workers at a DNT manufacturing plant. Samples were analyzed for 2,4- and 2,6-DNT and putative metabolites by gas chromatography-mass spectrometry. Urine from workers exposed to DNT contained 2,4- and 2,6-DNT, 2,4- and 2,6-dinitrobenzoic acid, 2,4- and 2,6-dinitrobenzyl glucuronide, 2-amino-4-nitrobenzoic acid, and 2-(N-acetyl)amino-4-nitrobenzoic acid. Excretion of these metabolites peaked near the end of the workshift, but declined to either very low or undetectable concentrations by the start of work the following day. The calculated half-times for elimination of total DNT-related material detected in urine ranged from 1.0 to 2.7 hr, and those of individual metabolites from 0.8 to 4.5 hr. The most abundant metabolites were 2,4-dinitrobenzoic acid and 2-amino-4-nitrobenzoic acid, collectively accounting for 74 to 86% of the DNT metabolites detected. The data indicate that urinary metabolites of DNT in humans are qualitatively similar to those found in rats, but quantitative differences exist in the relative amounts of each metabolite excreted.

All three dinitrobenzene (DNB) isomers cause methemoglobinemia, but only 1,3-DNB produces testicular toxicity in rats. In order to determine whether major differences exist in the routes of DNB metabolism, male Fischer-344 rats were given an oral dose (0.15 mmol/kg) of 14C-labeled 1,2-, 1,3-, or 1,4-DNB, and excreta were collected over 48 hr. Elimination of radiolabel was rapid; 85%, 60%, and 75% of the 1,2-, 1,3-, and 1,4-DNB dose was recovered in 24 hr, respectively. Urine was the primary route of excretion, accounting for 82% of the total dose of 1,2-DNB and 75% of the dose of 1,4-DNB after 48 hr. Radiolabel from 1,3-DNB was excreted to a slightly lesser extent in the urine (63% of the dose). A greater portion of radiolabel was excreted in the feces than with the other isomers (18% of total dose, compared to 8% and 9% with 1,2-DNB and 1,4-DNB, respectively). The major urinary metabolites of 1,2-DNB were S-(2-nitrophenyl)-N-acetylcysteine (42% of the dose), 2-nitroaniline-N-glucuronide (4%), 4-amino-3-nitrophenylsulfate (17%), 2-amino-3-nitrophenylsulfate (1.5%), and 2-(N-hydroxylamino)nitrobenzene (1-2%). The major urinary metabolites of 1,3-DNB were 3-aminoacetanilide (22%), 4-acetamidophenylsulfate (6%), 1,3-diacetamidobenzene (7%), and 3-nitroaniline-N-glucuronide (4%). The major metabolites of 1,4-DNB were 2-amino-5-nitrophenylsulfate (35%), S-(4-nitrophenyl)-N-acetylcysteine (13%), and 1,4-diacetamidobenzene (7%). These results suggest that the DNB isomers are primarily metabolized by nitro group reduction and conjugation with glutathione. The testicular toxicant 1,3-DNB was apparently metabolized exclusively by reduction.