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The number of immigrants and refugees in the United States is growing, yet many trainees and clinicians feel unprepared to manage the diverse needs of this population. This perspective piece describes the development of the Immigrant Partnership and Advocacy Curricular Kit (I-PACK) by the Midwest Consortium of Global Child Health Educators. I-PACK is an adjunct to the Consortiums sugarprep.org global health curricular materials. Using Kerns six-step approach to curriculum development, they developed eight modules in immigrant and refugee health that incorporate interactive learning activities. The I-PACK was launched as an open-access resource in September 2020. As of September 2021, the curriculum has been freely available at sugarprep.org/i-pack and downloaded from educators in 15 countries. The I-PACK curriculum can address a growing need in medical education to empower learners and clinicians to provide competent and compassionate care for immigrants and refugees.

Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic cause of renal failure. For several decades, ADPKD was regarded as an adult-onset disease. In the past decade, it has become more widely appreciated that the disease course begins in childhood. However, evidence-based guidelines on how to manage and approach children diagnosed with or at risk of ADPKD are lacking. Also, scoring systems to stratify patients into risk categories have been established only for adults. Overall, there are insufficient data on the clinical course during childhood. We therefore initiated the global ADPedKD project to establish a large international pediatric ADPKD cohort for deep characterization. Methods: Global ADPedKD is an international multicenter observational study focusing on childhood-diagnosed ADPKD. This collaborative project is based on interoperable Web-based databases, comprising 7 regional and independent but uniformly organized chapters, namely Africa, Asia, Australia, Europe, North America, South America, and the United Kingdom. In the database, a detailed basic data questionnaire, including genetics, is used in combination with data entry from follow-up visits, to provide both retrospective and prospective longitudinal data on clinical, radiologic, and laboratory findings, as well as therapeutic interventions. Discussion: The global ADPedKD initiative aims to characterize in detail the most extensive international pediatric ADPKD cohort reported to date, providing evidence for the development of unified diagnostic, follow-up, and treatment recommendations regarding modifiable disease factors. Moreover, this registry will serve as a platform for the development of clinical and/or biochemical markers predicting the risk of early and progressive disease.

Presentation given as part of Sustainability Week 2019. Presenters included: Denny Cohcrane, Director of Office of Sustainability; Blake Bensman, Sustainability Manager; and Nick Quint, Transportation Network Manager.

BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic cause of renal failure. For several decades, ADPKD was regarded as an adult-onset disease. In the past decade, it has become more widely appreciated that the disease course begins in childhood. However, evidence-based guidelines on how to manage and approach children diagnosed with or at risk of ADPKD are lacking. Also, scoring systems to stratify patients into risk categories have been established only for adults. Overall, there are insufficient data on the clinical course during childhood. We therefore initiated the global ADPedKD project to establish a large international pediatric ADPKD cohort for deep characterization. METHODS: Global ADPedKD is an international multicenter observational study focusing on childhood-diagnosed ADPKD. This collaborative project is based on interoperable Web-based databases, comprising 7 regional and independent but uniformly organized chapters, namely Africa, Asia, Australia, Europe, North America, South America, and the United Kingdom. In the database, a detailed basic data questionnaire, including genetics, is used in combination with data entry from follow-up visits, to provide both retrospective and prospective longitudinal data on clinical, radiologic, and laboratory findings, as well as therapeutic interventions. DISCUSSION: The global ADPedKD initiative aims to characterize in detail the most extensive international pediatric ADPKD cohort reported to date, providing evidence for the development of unified diagnostic, follow-up, and treatment recommendations regarding modifiable disease factors. Moreover, this registry will serve as a platform for the development of clinical and/or biochemical markers predicting the risk of early and progressive disease.

Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic cause of renal failure. For several decades, ADPKD was regarded as an adult-onset disease. In the past decade, it has become more widely appreciated that the disease course begins in childhood. However, evidence-based guidelines on how to manage and approach children diagnosed with or at risk of ADPKD are lacking. Also, scoring systems to stratify patients into risk categories have been established only for adults. Overall, there are insufficient data on the clinical course during childhood. We therefore initiated the global ADPedKD project to establish a large international pediatric ADPKD cohort for deep characterization. Methods: Global ADPedKD is an international multicenter observational study focusing on childhood-diagnosed ADPKD. This collaborative project is based on interoperable Web-based databases, comprising 7 regional and independent but uniformly organized chapters, namely Africa, Asia, Australia, Europe, North America, South America, and the United Kingdom. In the database, a detailed basic data questionnaire, including genetics, is used in combination with data entry from follow-up visits, to provide both retrospective and prospective longitudinal data on clinical, radiologic, and laboratory findings, as well as therapeutic interventions. Discussion: The global ADPedKD initiative aims to characterize in detail the most extensive international pediatric ADPKD cohort reported to date, providing evidence for the development of unified diagnostic, follow-up, and treatment recommendations regarding modifiable disease factors. Moreover, this registry will serve as a platform for the development of clinical and/or biochemical markers predicting the risk of early and progressive disease.

Presentation given as part of Sustainability Week 2019. Presenters included: Denny Cohcrane, Director of Office of Sustainability; Blake Bensman, Sustainability Manager; and Nick Quint, Transportation Network Manager.

Fanconi-Bickel syndrome is a rare autosomal-recessive disorder caused by mutations in the SLC2A2 gene coding for the glucose transporter protein 2 (GLUT2). Major manifestations include hepatomegaly, glucose intolerance, post-prandial hypoglycaemia and renal disease that usually presents as proximal tubular acidosis associated with proximal tubule dysfunction (renal Fanconi syndrome). We report a patient harbouring a homozygous mutation of SLC2A2 who presented a dramatic exacerbation of metabolic acidosis in the context of a viral infection, owing to both ketosis and major urinary bicarbonate loss. The kidney biopsy revealed nuclear and cytoplasmic accumulation of glycogen in proximal tubule cells, a lack of expression of GLUT2, and major defects of key proteins of the proximal tubule such as megalin, cubilin and the B2 subunit of H+-ATPase. These profound alterations of the transport systems most likely contributed to proximal tubule alterations and profound bicarbonate loss

This brief communication analyzes the statistics and methods Lotka used to derive his inverse square law of scientific productivity from the standpoint of modern theory. It finds that he violated the norms of this theory by extremely truncating his data on the right. It also proves that Lotka himself played an important role in establishing the commonly used method of identifying power-law behavior by the R^2 fit to a regression line on a log-log plot that modern theory considers unreliable by basing the derivation of his law on this very method., Comment: 12 pages, 5 figures, 2 tables

National legislation requires America’s homeland security agencies to disrupt transnational human smuggling organizations capable of transporting terrorist travelers to all U.S. borders. Federal agencies have responded with programs targeting extreme-distance human smuggling networks that transport higher-risk immigrants known as special interest aliens (SIAs) from some 35 countries of interest in the Middle East, North Africa, and Asia where terrorist organizations operate. Yet ineffectiveness and episodic targeting are indicated, in part by continued migration from those countries to the U.S. southwestern border since 9/11. Should an attack linked to SIA smuggling networks occur, homeland security leaders likely will be required to improve counter-SIA interdiction or may choose to do so preemptively. This thesis asks how SIA smuggling networks function as systems and, based on this analysis, if their most vulnerable fail points can be identified for better intervention targeting. Using NVivo qualitative analysis software, the study examined 19 U.S. court prosecutions of SIA smugglers and other data to produce 20 overarching conclusions demonstrating how SIA smuggling functions. From these 20 conclusions, seven leverage points were extracted and identified for likely law enforcement intervention success. Fifteen disruption strategies, tailored to the seven leverage points, are recommended.

Angiosperms, http://name.umdl.umich.edu/IC-HERB00IC-X-1522540%5DMICH-V-1522540, https://quod.lib.umich.edu/cgi/i/image/api/thumb/herb00ic/1522540/MICH-V-1522540/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. Some materials may be protected by copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, please contact the Herbarium professional staff: herb-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu., https://www.lib.umich.edu/about-us/policies/copyright-policy

Angiosperms, http://name.umdl.umich.edu/IC-HERB00IC-X-1522540%5DMICH-V-1522540, https://quod.lib.umich.edu/cgi/i/image/api/thumb/herb00ic/1522540/MICH-V-1522540/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. Some materials may be protected by copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, please contact the Herbarium professional staff: herb-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu., https://www.lib.umich.edu/about-us/policies/copyright-policy

Fanconi-Bickel syndrome is a rare autosomal-recessive disorder caused by mutations in the SLC2A2 gene coding for the glucose transporter protein 2 (GLUT2). Major manifestations include hepatomegaly, glucose intolerance, post-prandial hypoglycaemia and renal disease that usually presents as proximal tubular acidosis associated with proximal tubule dysfunction (renal Fanconi syndrome). We report a patient harbouring a homozygous mutation of SLC2A2 who presented a dramatic exacerbation of metabolic acidosis in the context of a viral infection, owing to both ketosis and major urinary bicarbonate loss. The kidney biopsy revealed nuclear and cytoplasmic accumulation of glycogen in proximal tubule cells, a lack of expression of GLUT2, and major defects of key proteins of the proximal tubule such as megalin, cubilin and the B2 subunit of H(+)-ATPase. These profound alterations of the transport systems most likely contributed to proximal tubule alterations and profound bicarbonate loss.

Recently, scholars from a wide variety of disciplines, using a variety of scientific techniques, have begun to study the influence of attention, facial mimicry, and social context on emotional contagion. In this paper we will review the classic evidence documenting the role of attention, facial mimicry, and feedback in sparking primitive emotional contagion. Then we will discuss the new evidence which scholars have amassed to help us better understand the role of facial mimicry in fostering contagion and the ability to “read” others’ thoughts, feelings, and emotions. Finally, we will briefly speculate as to where future research might be headed.

Fanconi-Bickel syndrome is a rare autosomal-recessive disorder caused by mutations in the SLC2A2 gene coding for the glucose transporter protein 2 (GLUT2). Major manifestations include hepatomegaly, glucose intolerance, post-prandial hypoglycaemia and renal disease that usually presents as proximal tubular acidosis associated with proximal tubule dysfunction (renal Fanconi syndrome). We report a patient harbouring a homozygous mutation of SLC2A2 who presented a dramatic exacerbation of metabolic acidosis in the context of a viral infection, owing to both ketosis and major urinary bicarbonate loss. The kidney biopsy revealed nuclear and cytoplasmic accumulation of glycogen in proximal tubule cells, a lack of expression of GLUT2, and major defects of key proteins of the proximal tubule such as megalin, cubilin and the B2 subunit of H(+)-ATPase. These profound alterations of the transport systems most likely contributed to proximal tubule alterations and profound bicarbonate loss.

This paper presents proof that Google Scholar (GS) can construct documentary sets relevant for evaluating researchers' works. Nobelists in economics were the researchers under analysis, and two types of tests of the GS cites to their works were performed: distributional and semantic. Distributional tests found that the GS cites to the laureates' works conformed to the power-law model with an asymptote or "tail" conterminous with their h-index demarcating their core oeuvre, validating both GS and the h-index. Semantic tests revealed that their works highest in GS cites were on topics for which they were awarded the prize.

This paper uses the Yule-Simon model to estimate to what extent the work of chemistry Nobelists and Fields medalist mathematicians is incorporated into the knowledge corpus of their disciplines as measured by Google Scholar inlinks. Due to differences in the disciplines and prizes, it finds that the work of chemistry Nobelists is better incorporated than that of Fields medalists.

This paper presents a test of the validity of using Google Scholar to evaluate the publications of researchers by comparing the premises on which its search engine, PageRank, is based, to those of Garfield's theory of citation indexing. It finds that the premises are identical and that PageRank and Garfield's theory of citation indexing validate each other.

Atypical hemolytic uremic syndrome is often associated with mutations in genes encoding complement regulatory proteins and secondary disorders of complement regulation. Progression to kidney failure and recurrence with graft loss after kidney transplantation are frequent. The most common mutation is in the gene encoding complement factor H. Combined liver-kidney transplantation may correct this complement abnormality and prevent recurrence when the defect involves genes encoding circulating proteins that are synthesized in the liver, such as factor H or I. Good outcomes have been reported when surgery is associated with intensified plasma therapy. A consensus conference to establish treatment guidelines for atypical hemolytic uremic syndrome was held in Bergamo in December 2007. The recommendations in this article are the result of combined clinical experience, shared research expertise, and a review of the literature and registry information. This statement defines groups in which isolated kidney transplantation is extremely unlikely to be successful and a combined liver-kidney transplant is recommended and also defines those for whom kidney transplant remains a viable option. Although combined liver-kidney or isolated liver transplantation is the preferred therapeutic option in many cases, the gravity of risk associated with the procedure has not been eliminated completely, and assessment of risk and benefit requires careful and individual attention. Copyright © 2009 by the American Society of Nephrology.

National legislation requires America’s homeland security agencies to disrupt transnational human smuggling organizations capable of transporting terrorist travelers to all U.S. borders. Federal agencies have responded with programs targeting extreme-distance human smuggling networks that transport higher-risk immigrants known as special interest aliens (SIAs) from some 35 countries of interest in the Middle East, North Africa, and Asia where terrorist organizations operate. Yet ineffectiveness and episodic targeting are indicated, in part by continued migration from those countries to the U.S. southwestern border since 9/11. Should an attack linked to SIA smuggling networks occur, homeland security leaders likely will be required to improve counter-SIA interdiction or may choose to do so preemptively. This thesis asks how SIA smuggling networks function as systems and, based on this analysis, if their most vulnerable fail points can be identified for better intervention targeting. Using NVivo qualitative analysis software, the study examined 19 U.S. court prosecutions of SIA smugglers and other data to produce 20 overarching conclusions demonstrating how SIA smuggling functions. From these 20 conclusions, seven leverage points were extracted and identified for likely law enforcement intervention success. Fifteen disruption strategies, tailored to the seven leverage points, are recommended., Outstanding Thesis, Manager and Program Specialist, Texas Department of Public Safety, Intelligence and Counterterrorism Division, Approved for public release; distribution is unlimited.

Fanconi-Bickel syndrome is a rare autosomal-recessive disorder caused by mutations in the SLC2A2 gene coding for the glucose transporter protein 2 (GLUT2). Major manifestations include hepatomegaly, glucose intolerance, post-prandial hypoglycaemia and renal disease that usually presents as proximal tubular acidosis associated with proximal tubule dysfunction (renal Fanconi syndrome). We report a patient harbouring a homozygous mutation of SLC2A2 who presented a dramatic exacerbation of metabolic acidosis in the context of a viral infection, owing to both ketosis and major urinary bicarbonate loss. The kidney biopsy revealed nuclear and cytoplasmic accumulation of glycogen in proximal tubule cells, a lack of expression of GLUT2, and major defects of key proteins of the proximal tubule such as megalin, cubilin and the B2 subunit of H+-ATPase. These profound alterations of the transport systems most likely contributed to proximal tubule alterations and profound bicarbonate loss