High level of novelty under the hood of convergent evolution.

Little is known about the extent to which species use homologous regulatory architectures to achieve phenotypic convergence. By characterizing chromatin accessibility and gene expression in developing wing tissues, we compared the regulatory architecture of convergence between a pair of mimetic butterfly species. Although a handful of color pattern genes are known to be involved in their convergence, our data suggest that different mutational paths underlie the integration of these genes into wing pattern development. This is supported by a large fraction of accessible chromatin being exclusive to each species, including the de novo lineage-specific evolution of a modular optix enhancer. These findings may be explained by a high level of developmental drift and evolutionary contingency that occurs during the independent evolution of mimicry.

SARS-CoV-2/COVID-19 and its relationship with NOD2 and ubiquitination.

COVID-19 infection activates the immune system to cause autoimmune and autoinflammatory diseases. We provide a comprehensive review of the relationship between SARS-CoV-2, NOD2 and ubiquitination. COVID-19 infection partly results from host inborn errors and genetic factors and can lead to autoinflammatory disease. The interaction between defective NOD2 and viral infection may trigger NOD2-associated disease. SARS-CoV-2 can alter UBA1 and abnormal ubiquitination leading to VEXAS syndrome. Both NOD2 and ubiquitination play important roles in controlling inflammatory process. Receptor interacting protein kinase 2 is a key component of the NOD2 activation pathway and becomes ubiquitinated to recruit downstream effector proteins. NOD2 mutations result in loss of ubiquitin binding and increase ligand-stimulated NOD2 signaling. During viral infection, mutations of either NOD2 or UBA1 genes or in combination can facilitate autoinflammatory disease. COVID-19 infection can cause autoinflammatory disease. There are reciprocal interactions between SARS-CoV-2, NOD2 and ubiquitination.

Hereditary pancreatitis: An updated review in pediatrics.

Hereditary Pancreatitis (HP) has emerged as a significant cause of acute, acute recurrent and chronic pancreatitis in the pediatric population. Given that it presents similarly to other causes of pancreatitis, a positive family history and/or isolation of a gene mutation are vital in its designation. Inheritance patterns remain complex, but mutations involving the PRSS1, SPINK1, CFTR and CTRC genes are commonly implicated. Since being first described in 1952, dozens of genetic alterations that modify the action of pancreatic enzymes have been identified. Among children, these variants have been isolated in more than 50% of patients with chronic pancreatitis. Recent research has noted that such mutations in PRSS1, SPINK1 and CFTR genes are also associated with a faster progression from acute pancreatitis to chronic pancreatitis. Patients with HP are at increased risk of developing diabetes mellitus, exocrine pancreatic insufficiency, and pancreatic adenocarcinoma. Management follows a multi-disciplinary approach with avoidance of triggers, surveillance of associated conditions, treatment of pancreatic insufficiency and use of endoscopic and surgical interventions for complications. With significant sequela, morbidity and a progressive nature, a thorough understanding of the etiology, pathophysiologic mechanisms, diagnostic evaluation, current management strategies and future research considerations for this evolving disease entity in pediatrics is warranted.

Heliconius butterflies: a window into the evolution and development of diversity.

Butterflies have become prominent models for studying the evolution and development of phenotypic variation. In Heliconius, extraordinary within species divergence and between species convergence in wing color patterns has driven decades of comparative genetic studies. However, connecting genetic patterns of diversification to the molecular mechanisms of adaptation has remained elusive. Recent studies are bridging this gap between genome and function and have driven substantial advances in deciphering the genetic architecture of diversification in Heliconius. While only a handful of large-effect genes were initially identified in the diversification of Heliconius color patterns, recent experiments have begun to unravel the underlying gene regulatory networks and how these have evolved. These results reveal an evolutionary story of many interacting loci and partly independent genetic architectures that underlie convergent evolution.

Interplay between Developmental Flexibility and Determinism in the Evolution of Mimetic Heliconius Wing Patterns.

To what extent can we predict how evolution occurs? Do genetic architectures and developmental processes canalize the evolution of similar outcomes in a predictable manner? Or do historical contingencies impose alternative pathways to answer the same challenge? Examples of Müllerian mimicry between distantly related butterfly species provide natural replicates of evolution, allowing us to test whether identical wing patterns followed parallel or novel trajectories. Here, we explore the role that the signaling ligand WntA plays in generating mimetic wing patterns in Heliconius butterflies, a group with extraordinary mimicry-related wing pattern diversity. The radiation is relatively young, and numerous cases of wing pattern mimicry have evolved within the last 2.5-4.5 Ma. WntA is an important target of natural selection and is one of four major effect loci that underlie much of the pattern variation in the group. We used CRISPR/Cas9 targeted mutagenesis to generate WntA-deficient wings in 12 species and a further 10 intraspecific variants, including three co-mimetic pairs. In all tested butterflies, WntA knockouts affect pattern broadly and cause a shift among every possible scale cell type. Interestingly, the co-mimics lacking WntA were very different, suggesting that the gene networks that pattern a wing have diverged considerably among different lineages. Thus, although natural selection channeled phenotypic convergence, divergent developmental contexts between the two major Heliconius lineages opened different developmental routes to evolve resemblance. Consequently, even under very deterministic evolutionary scenarios, our results underscore a surprising unpredictability in the developmental paths underlying convergence in a recent radiation.

Meandering Main Pancreatic Duct in Association with Choledochal Cysts and Acute Pancreatitis in Pediatrics.

Meandering main pancreatic duct (MMPD) is an uncommon anomaly of the main pancreatic duct characterized by an abnormal curvature at the pancreatic head region. This variant can be diagnosed on imaging, particularly magnetic resonance cholangiopancreatography (MRCP). Although its clinical significance remains debatable, recent research suggests an association with recurrent acute pancreatitis. To our knowledge, no pediatric cases of acute or recurrent acute pancreatitis have been attributed to the presence of MMPD. In this article, we report on two patients. The first case is of a 15-year-old girl with MMPD discovered on investigation of idiopathic acute pancreatitis. The second case is of a 5-year-old boy who presented with his second episode of acute pancreatitis. In this patient, MRCP imaging revealed MMPD and type IVA choledochal cyst. With appropriate care, both patients experienced clinical improvement with resolution of abdominal pain. This article highlights MMPD as a distinct entity that should be considered in pediatric patients with recurrent attacks of acute pancreatitis. This report also describes the first association of MMPD with choledochal cysts. [Pediatr Ann. 2019;48(10):e412-e416.].

Hypophosphatemia in a Malnourished Child: When Renal Fanconi Syndrome Does Not Stand for Refeeding Syndrome.

Refeeding syndrome is diagnosed based on the onset of multiple laboratory abnormalities (most commonly hypophosphatemia) and clinical signs in the setting of nutrition rehabilitation of malnourished patients. Because definitions are not uniform, a broad differential diagnosis should always include renal tubular dysfunction. Our report details a 3 year-old child with undiagnosed renal tubular dysfunction who presented with the clinical picture of refeeding syndrome with refractory electrolyte abnormalities. A diagnosis of renal Fanconi syndrome was made after urinalysis that revealed glucosuria and urine electrolyte losses. Thus, urinalysis can aid in making a positive diagnosis of refeeding syndrome.

The Mesentery, Systemic Inflammation, and Crohn's Disease.

Initially thought to be a structure that only provided support to the abdominal contents, the mesentery has now gained special attention in the scientific community. The new approach of studying the mesentery as an individual organ has highlighted its importance in the development of local and systemic inflammatory diseases and its potential role in Crohn's disease. Its topographical relationship with the intestine in the setting of active inflammation and "creeping fat" is possibly one of the most important arguments for including the mesentery as an important factor in the pathogenesis of Crohn's disease. In this review, we discuss the importance of the mesentery from the anatomical and embryological standpoints. We also will summarize data on mesenteric inflammation in patients with Crohn's disease. The significance of the mesentery in systemic inflammatory syndromes will be discussed, and we provide an overview of primary inflammatory disorders of the mesentery. Finally, we discuss surgical approaches for patients requiring resection for Crohn's disease that incorporate mesenteric factors, pointing out recent data suggesting that these have the potential for improving outcomes and reducing disease recurrence.10.1093/ibd/izy201_video1izy201.video15794169491001.

Scarlet fever associated with hepatitis in pediatrics. A case report. / Scarlet fever associated with hepatitis in pediatrics. A case report.

INTRODUCTION: Scarlet fever is a common illness in pediatrics caused by group A beta-hemolytic strep tococcus (GABHS), which usually occurs after an episode of pharyngitis, and has an overall excellent prognosis. Hepatitis secondary to scarlet fever is a rare complication described in adults and even less frequently in children. Our objective was to describe a case of hepatitis secondary to scarlet fever in a pediatric patient. CLINICAL CASE: A 12-year-old male with scarlet fever presented with a 4-day history of jaundice, dark urine, and decreased appetite. Laboratory tests revealed elevated liver enzy mes and total and direct bilirubin levels, and negative studies for hepatitis A, B and C, Epstein Barr virus, parvovirus B19, adenovirus, cytomegalovirus, human herpes virus-6, and herpes simplex virus 1 and 2. Abdominal ultrasound examination was normal. DISCUSSION: The pathogenesis of scarlet fever associated hepatitis remains unclear. Streptococcal pyrogenic exotoxin mediated cellular injury via cytokine production has been proposed as a possible mechanism of hepatotoxicity in GABHS infections. CONCLUSION: Hepatitis secondary to scarlet fever remains a rare but benign entity, with complete recovery expected over weeks to months.

Scarlet fever associated with hepatitis in pediatrics: a case report / Hepatitis asociada a escarlatina en pediatría: reporte de caso

INTRODUCCIÓN: La escarlatina es una enfermedad común en Pediatría, causada por Estreptococo beta hemolítico grupo A (SBHGA), la cual generalmente se presenta después de un episodio de faringitis, y con excelente pronóstico general. La hepatitis secundaria a escarlatina es una complicación, descrita muy rara vez en niños. Nuestro objetivo fue reportar la ocurrencia de hepatitis secundaria a escarlati na en un paciente pediátrico. CASO CLÍNICO: Varón de 12 años cursando escarlatina, quien se presentó con una historia de 4 días de ictericia, coluria y disminución del apetito. Los exámenes de laboratorio revelaron elevación de las transaminasas y de los niveles de bilirrubina total y directa, y estudios vira les negativos para Hepatitis A, B y C, Virus de Epstein Barr, Parvovirus B19, Citomegalovirus, Virus Herpes 6 y Herpes simplex 1 y 2. Ecografía abdominal fue normal. DISCUSIÓN: La hepatitis es una complicación inhabitual de la escarlatina, cuya patogénesis aún no está clara. La producción de citoquinas a través del daño celular mediado por la exotoxina pirógena estreptocócica, se ha propuesto como un posible mecanismo de hepatotoxicidad en infecciones por SBHGA. CONCLUSIÓN: La hepati tis asociada a escarlatina continúa siendo una entidad rara, pero de curso benigno, con recuperación plena en semanas a meses.

INTRODUCTION: Scarlet fever is a common illness in pediatrics caused by group A beta-hemolytic streptococcus (GABHS), which usually occurs after an episode of pharyngitis, and has an overall excellent prognosis. Hepatitis secondary to scarlet fever is a rare complication described in adults and even less frequently in children. Our objective was to describe a case of hepatitis secondary to scarlet fever in a pediatric patient. CLINICAL CASE: A 12-year-old male with scarlet fever presented with a 4-day history of jaundice, dark urine, and decreased appetite. Laboratory tests revealed elevated liver enzy mes and total and direct bilirubin levels, and negative studies for hepatitis A, B and C, Epstein Barr virus, parvovirus B19, adenovirus, cytomegalovirus, human herpes virus-6, and herpes simplex virus 1 and 2. Abdominal ultrasound examination was normal. DISCUSSION: The pathogenesis of scarlet fever associated hepatitis remains unclear. Streptococcal pyrogenic exotoxin mediated cellular injury via cytokine production has been proposed as a possible mechanism of hepatotoxicity in GABHS infections. CONCLUSION: Hepatitis secondary to scarlet fever remains a rare but benign entity, with complete recovery expected over weeks to months.

The Characterization of Monoclonal Antibodies to Mouse TLT-1 Suggests That TLT-1 Plays a Role in Wound Healing.

Platelets play a vital role in hemostasis and inflammation. The membrane receptor TREM-like transcript-1 (TLT-1) is involved in platelet aggregation, bleeding, and inflammation, and it is localized in the α-granules of platelets. Upon platelet activation, TLT-1 is released from α-granules both in its transmembrane form and as a soluble fragment (sTLT-1). Higher levels of sTLT-1 have been detected in the plasma of patients with acute inflammation or sepsis, suggesting an important role for TLT-1 during inflammation. However, the roles of TLT-1 in hemostasis and inflammation are not well understood. We are developing the mouse model of TLT-1 to mechanistically test clinical associations of TLT-1 in health and disease. To facilitate our studies, monoclonal murine TLT-1 (mTLT-1) antibodies were produced by the immunization of a rabbit using the negatively charged region of the mTLT-1 extracellular domain 122PPVPGPREGEEAEDEK139. In the present study, we demonstrate that two selected clones, 4.6 and 4.8, are suitable for the detection of mTLT-1 by western blot, immunoprecipitation, immunofluorescent staining, flow cytometry and inhibit platelet aggregation in aggregometry assays. In addition, we found that the topical administration of clone 4.8 delayed the wound healing process in an experimental burn model. These results suggest that TLT-1 plays an important role in wound healing and because both clones specifically detect mTLT-1, they are suitable to further develop TLT-1 based models of inflammation and hemostasis in vivo.

Cryptosporidium diagnosed on endoscopic biopsy in a paediatric patient with inflammatory bowel disease.

Cryptosporidium, a parasitic infection commonly associated with diarrhoea, may be difficult to differentiate from a flare in patients with inflammatory bowel disease and can lead to unnecessary therapy and increase in morbidity and mortality. We report the case of a paediatric patient who had substantial stool output requiring significant fluid resuscitation and who was later diagnosed with cryptosporidium on endoscopic biopsy. Diagnostic work up for cryptosporidium should be strongly considered when a patient presents with a flare involving massive stool output.

[Pancreatitis, genes and islet cells auto transplant; updates and new horizons]. / Pancreatitis, genes y autotrasplante de islotes; actualizaciones y nuevos horizontes.

Pancreatitis is an inflammation of the pancreas that can progress from an acute presentation to an acute recurring presentation and eventually to chronic pancreatitis, which is characterized by irreversible morphological changes and scarring of the pancreas. The entity known as hereditary pancreatitis has been recognized in the literature for years and certainly the discovery of the PRSS1 gene in 1996 marked the beginning of a new era of genetic discoveries associated with the disease. Since then, multiple genes have been described as the causing agents of pancreatitis or disease modifiers, some of the most important ones being the PRSS1, SPINK1, CFTR, CASR, CTRC, CLDN2, and CPA1. The patient selection process for genetic testing should be guided by the current experts' recommendations and should meet specific corresponding criteria. Once the diagnosis has been made, treatment should be tailored to each patient's particular needs. Certainly, the advent of the total pancreatectomy with auto islet cell transplantation, which has the main goal to improve the pain caused by the chronic pancreatitis and simultaneously reduce the severity of the pancreatectomy induced diabetes, is an attractive alternative in the treatment and management of patient with a diagnosis of hereditary pancreatitis. However, strict criteria and an interdisciplinary management are essential since this surgery is irreversible and carries lifetime health consequences that all patients must be aware of and the medical team must be able to early recognize these and treat accordingly. However, there are many potential areas in this field for more, better and forefront research to be developed aiming for a better understanding of the disease process and for the development of a cure.

Pancreatitis, genes y autotrasplante de islotes: actualizaciones y nuevos horizontes / Pancreatitis, genes and islet cells auto transplant: updates and new horizons

La pancreatitis es una inflamación del páncreas que puede progresar de una presentación aguda, a una presentación aguda recurrente y eventualmente a pancreatitis crónica, caracterizada por cambios morfológicos y formación de cicatriz los cuales son irreversibles. La entidad conocida como pancreatitis hereditaria ha sido reconocida en la literatura por años y ciertamente el hallazgo del gen PRSS1 en 1996 marcó el inicio de una era de descubrimientos genéticos asociados a dicha enfermedad. Desde entonces, múltiples genes han sido descritos como causa de pancreatitis hereditaria o modificadores de la enfermedad, entre los que se destacan el PRSS1, SPINK1, CFTR, CASR, CTRC, CLDN2 y CPA1 entre otros. La selección de pacientes a la que se le va a practicar los estudios genéticos correspondientes debe ser guiada por las recomendaciones de los expertos y debe cumplir con los criterios correspondientes. El tratamiento, una vez hecho el diagnóstico, debe ser adaptado en base a las necesidades particulares de cada paciente. Ciertamente, el advenimiento de la pancreatectomía total con auto trasplante, cuyo principal objetivo es aliviar el dolor ocasionado por la pancreatitis crónica a la vez que se reduce la severidad de la diabetes inducida por la pancreatectomía, es una alternativa atractiva en el tratamiento y manejo de pacientes con diagnóstico de pancreatitis hereditaria. Sin embargo, estrictos criterios y un manejo interdisciplinario son esenciales ya que éste es un procedimiento irreversible y tiene consecuencias médicas por el resto de la vida que todo paciente tiene que conocer y que a su vez, el equipo médico debe saber identificar y tratar a tiempo. Sin embargo, existen muchas áreas potenciales en este campo para investigaciones que sean mayores, mejores y a la vanguardia para lograr un mejor entendimiento y desarrollar potenciales curas para esta enfermedad

Pancreatitis is an inflammation of the pancreas that can progress from an acute presentation to an acute recurring presentation and eventually to chronic pancreatitis, which is characterized by irreversible morphological changes and scarring of the pancreas. The entity known as hereditary pancreatitis has been recognized in the literature for years and certainly the discovery of the PRSS1 gene in 1996 marked the beginning of a new era of genetic discoveries associated with the disease. Since then, multiple genes have been described as the causing agents of pancreatitis or disease modifiers, some of the most important ones being the PRSS1, SPINK1, CFTR, CASR, CTRC, CLDN2, and CPA1. The patient selection process for genetic testing should be guided by the current experts’ recommendations and should meet specific corresponding criteria. Once the diagnosis has been made, treatment should be tailored to each patient’s particular needs. Certainly, the advent of the total pancreatectomy with auto islet cell transplantation, which has the main goal to improve the pain caused by the chronic pancreatitis and simultaneously reduce the severity of the pancreatectomy induced diabetes, is an attractive alternative in the treatment and management of patient with a diagnosis of hereditary pancreatitis. However, strict criteria and an interdisciplinary management are essential since this surgery is irreversible and carries lifetime health consequences that all patients must be aware of and the medical team must be able to early recognize these and treat accordingly. However, there are many potential areas in this field for more, better and forefront research to be developed aiming for a better understanding of the disease process and for the development of a cure

Hereditary Pancreatitis.

A 13-year-old boy with a strong family history of hereditary pancreatitis was found to have a PRSS1 mutation after being tested at age 5 years during his first documented incident of pancreatitis. Since then, a multidisciplinary team has been treating him for the diagnosis of hereditary pancreatitis. His pain episodes increased in severity over the past several months such that the pain began to severely interfere with his daily life. After extensive discussion, a total pancreatectomy with auto islet cell transplant was performed. He is now pain free and does not require any insulin. This leads us to the questions of what is hereditary pancreatitis and how is it diagnosed? What are the management and follow-up strategies needed for these patients? This article addresses these questions and informs the reader about this diagnosis and the importance of having a high index of clinical suspicion.

Recurrent Pediatric Perianal Swelling.

Pediatric inflammatory bowel disease is a chronic gastrointestinal disease consisting of Crohn's disease (CD) and ulcerative colitis (UC). Both disease processes can share similar clinical symptoms including abdominal pain, diarrhea, hematochezia, and weight loss; CD can also be complicated by penetrating and fistulizing disease. Perianal skin tags, perianal abscesses, recto-cutaneous fistulae, and rectal stenosis are among the phenotypic characteristics of perianal CD. Current treatment strategies are focused on the surgical drainage of abscesses and the closure of fistulous tracts as well as controlling intestinal inflammation with the use of immunomodulators (6-mercaptopurine and methotrexate) and biologics (infliximab and adalimumab). Current guidelines by the American Gastroenterology Association and the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition recommend a combination of surgical intervention and medical management for the treatment of perianal CD.

Escala de Calgary para el diagnóstico del síncope vasovagal. Estudio de pruebas diagnósticas / Calgary score for the diagnosis of vasovagal syncope. Diagnostic tests study

Objetivo: Evaluar la utilidad de la escala de Calgary en el diagnóstico de síncope vasovagal comparada con los resultados de la prueba de mesa inclinada (Tilt test) bajo protocolo sensibilizado con medicamentos. Metodología: Estudio prospectivo de pruebas diagnósticas en pacientes con sospecha de síncope vasovagal sometidos a prueba de mesa inclinada (Tilt test) con vasodilatación inducida con nitroglicerina por vía sublingual. Se incluyeron pacientes mayores de 18 años de edad y se excluyeron pacientes con cardiopatía estructural documentada. Resultados: Se analizaron 100 pacientes, promedio de 48,7 años (DE 19,7), 69% de género femenino y 4% residentes en área rural. La mediana de síncopes al momento del Tilt test fue de 5 (RIQ 2-15) con presentación del primer episodio a los 41 años (RIQ 21-57), en el 52% de los pacientes no se identificaron desencadenantes y las manifestaciones clínicas referidas en los episodios previos al Tilt test fueron diaforesis (58%), palidez (55%), mareo (70%), palpitaciones (50%) y náuseas (42%); durante el Tilt test se reportaron mareo (65%), diaforesis (19%), náuseas (18%) y visión borrosa (18%). Se obtuvo una sensibilidad del 77,7% (IC 95%: 66,7-88,8) y una especificidad del 40,5% (IC 95%: 23,3-57,7) para la escala de Calgary. Conclusiones: Debido a su buena sensibilidad y fácil aplicación, la escala de Calgary es un instrumento útil para el abordaje diagnóstico de pacientes con sospecha de síncope vasovagal y corazón estructuralmente sano, especialmente en menores de 50 años de edad.

Objective: Evaluate the utility of Calgary score for the diagnosis of vasovagal syncope compared with the results of the Tilt table test using sensibilized protocol with medicines. Methodology: Prospective study of diagnostic tests in patients with suspected diagnostic of vasovagal syncope who underwent tilt table test with induced vasodilation with sublingual nitroglycerin. Patients over 18 years were included and patients with documented structural heart disease were excluded. Results: 100 patients were analyzed, averaging 48.7 years of age (SD 19.7), 69% of feminine genre and 4% residents in rural area. Medium of syncope at the moment of tilt table test was 5 (IQR 2-15), with presentation of first episode at 41 years (IQR 21-57), in 52% of the patients triggers were not identified and the clinical manifestations referred in episodes previous to Tilt test were diaphoresis (58%), pallor (55%), dizziness (70%), palpitations (50%) and nausea (42%); during the test dizziness (65%), diaphoresis (19%), nausea (18%) and blurred vision (18%) were reported. A sensitivity of 77.7% was obtained (95% CI 88.8 66.7) and specificity of 40.5% (95% CI 23.3 - 57.7) for the Calgary score. Conclusions: Due to its high sensitivity and easy application, the Calgary score is a useful diagnostic approach instrument for patients with suspected vasovagal syncope and who have a structurally healthy heart, especially in those younger than 50 years.

Measuring Computed Tomography Scanner Variability of Radiomics Features.

OBJECTIVES: The purpose of this study was to determine the significance of interscanner variability in CT image radiomics studies. MATERIALS AND METHODS: We compared the radiomics features calculated for non-small cell lung cancer (NSCLC) tumors from 20 patients with those calculated for 17 scans of a specially designed radiomics phantom. The phantom comprised 10 cartridges, each filled with different materials to produce a wide range of radiomics feature values. The scans were acquired using General Electric, Philips, Siemens, and Toshiba scanners from 4 medical centers using their routine thoracic imaging protocol. The radiomics feature studied included the mean and standard deviations of the CT numbers as well as textures derived from the neighborhood gray-tone difference matrix. To quantify the significance of the interscanner variability, we introduced the metric feature noise. To look for patterns in the scans, we performed hierarchical clustering for each cartridge. RESULTS: The mean CT numbers for the 17 CT scans of the phantom cartridges spanned from -864 to 652 Hounsfield units compared with a span of -186 to 35 Hounsfield units for the CT scans of the NSCLC tumors, showing that the phantom's dynamic range includes that of the tumors. The interscanner variability of the feature values depended on both the cartridge material and the feature, and the variability was large relative to the interpatient variability in the NSCLC tumors for some features. The feature interscanner noise was greatest for busyness and least for texture strength. Hierarchical clustering produced different clusters of the phantom scans for each cartridge, although there was some consistent clustering by scanner manufacturer. CONCLUSIONS: The variability in the values of radiomics features calculated on CT images from different CT scanners can be comparable to the variability in these features found in CT images of NSCLC tumors. These interscanner differences should be considered, and their effects should be minimized in future radiomics studies.

A 15-year-old boy with abdominal pain, growth retardation, and anemia secondary to Helicobacter pylori-associated peptic ulcer.

A 15-year-old boy with abdominal pain, growth retardation, and symptomatic anemia requiring blood transfusion was seen by a gastroenterologist and found to have a large ulcerated, fungating, and actively bleeding mass in his stomach. Initially, the patient was screened for Helicobacter pylori and found to be negative, so there was concern for malignancy after multiple endoscopic procedures. The patient did not respond to initial ulcer treatment and immediately prior to scheduled partial gastrectomy, additional tissue sections from the initial biopsy were stained for H. pylori and rare positive staining organisms were found. The test was positive, and the patient was started empirically on treatment to which he responded and ultimately recovered fully. Gastrectomy was not performed, and following treatment, the ulcer, anemia, and poor growth resolved.

Overview of neuropathy associated with taxanes for the treatment of metastatic breast cancer.

Taxanes are an established option in the standard treatment paradigm for patients with metastatic breast cancer (MBC). Neuropathy is a common, dose-limiting side effect of taxane therapy that is often managed by dose reductions and delays. The severity, time to onset, and improvement in neuropathy are important considerations for patient management and vary among currently approved taxanes. The rate of grade ≥3 neuropathy with taxanes has been shown to be dose and schedule dependent; however, time to improvement to grade ≤1 is typically shorter for nab-paclitaxel than for other taxanes in patients with MBC. Many tools for assessing patient-reported neuropathy exist. Because MBC is incurable and patient quality of life must be critically considered when making treatment decisions, there is a need for more prospective trials to assess patient-reported neuropathy. Validated predictors of taxane-related neuropathy may play an important role in treatment decisions in the future. This review will focus on the toxicity profile (i.e., neuropathy) of each of the taxanes used in the treatment of MBC, will provide updates on tools used for the assessment of neuropathy, and will highlight newly discovered predictors of taxane-related neuropathy.