Define and describe the roles and responsibilities of the Chief Academic Officer (CAO) in the creation of sustainable interprofessional learning experiences (ILE) sponsored or co-sponsored through Academic Health Centers (AHCs).

Clinical AnatomyVolume 23, Issue 1 p. 129-129 Book Review Atlas of Descriptive Histology by Michael H. Ross, Wojciech Pawlina, and Todd A. Barnash Robert M. Klein, Corresponding Author Robert M. Klein rklein@kumc.edu Department of Anatomy and Cell Biology, University of Kansas, School of Medicine, Kansas City, KansasDepartment of Anatomy and Cell Biology, Mail Stop # 3038, University of Kansas, School of Medicine, 3901 Rainbow Blvd., Kansas City, Kansas 66160, USASearch for more papers by this author Robert M. Klein, Corresponding Author Robert M. Klein rklein@kumc.edu Department of Anatomy and Cell Biology, University of Kansas, School of Medicine, Kansas City, KansasDepartment of Anatomy and Cell Biology, Mail Stop # 3038, University of Kansas, School of Medicine, 3901 Rainbow Blvd., Kansas City, Kansas 66160, USASearch for more papers by this author First published: 13 November 2009 https://doi.org/10.1002/ca.20891AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume23, Issue1January 2010Pages 129-129 RelatedInformation

It was not until the twentieth century that pain was considered a disease. Before that it was managed medically as a symptom. The motivations for declaring chronic pain a disease, whether of the body or of the brain, include increasing its legitimacy as clinical problem and research focus worthy of attention from healthcare and research organizations alike. But 1 problem with disease concepts is that having a disease favors medical solutions and tends to reduce patient participation. We argue that chronic pain, particularly chronic primary pain (recently designated a first tier pain diagnosis in International Diagnostic Codes 11), is a learned state that is not intransigent even if it has biological correlates. Chronic pain is sometimes a symptom, and may sometimes be its own disease. But here we question the value of a disease focus for much of chronic pain for which patient involvement is essential, and which may need a much broader societal approach than is suggested by the disease designation.This article examines whether designating chronic pain a disease of the body or brain is helpful or harmful to patients. Can the disease designation help advance treatment, and is it needed to achieve future therapeutic breakthrough? Or does it make patients over-reliant on medical intervention and reduce their engagement in the process of recovery?

Human studies of unexplained cerebral palsy (CP) suggest an association with maternal infection. We used an established model of maternal infection, lipopolysaccharide (LPS) administration, to investigate the molecular changes in the fetal brain that may link maternal infection and CP. We compared gene expression in brains from mouse pups exposed to LPS in utero to those from saline-treated controls. Dams were injected with 50μg LPS or saline on E18 with surgical delivery from 0.5 to 6h later. Differential gene expression was analyzed in the whole mouse brain using RT-PCR. When compared to control mice, pups exposed to LPS showed increased expression of pro-inflammatory genes monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), and interleukin-1β (IL-1β), as well as VEGF, a regulator of vascular development and permeability, the anti-apoptotic protein Y-box-binding protein-1 (YB-1), and the neuronal differentiation factor necdin. LPS-exposed mice also showed downregulation of semaphorin 5b and groucho, involved in axon guidance and neurogenesis, respectively, providing evidence that LPS may disrupt normal developmental pathways. These data suggest possible mechanisms for adverse neurological outcomes following maternal infection involving elevated cytokine levels and altered expression of developmental genes in the fetal brain.

Key Words: clinical skillsfundoscopyteaching and learningKey Words: appraisalgeneral practice non-principals

Objectives.—We examined changes in the serotonin system across the estrous cycle in trigeminal ganglia of female rodents to determine which components are present and which are regulated by the variations in levels of ovarian steroids that occur during the estrous cycle.Background.—Migraine is 2–3 times more prevalent in women than in men and attacks are often timed with the menstrual cycle, suggesting a mechanistic link with ovarian steroids. Serotonin has been implicated in the pathogenesis of migraine, and the effectiveness of triptans, selective 5HT‐1B/D/F agonists, has provided further support for this concept. It is not known whether serotonin, its rate‐limiting enzyme tryptophan hydroxylase (TPH), or its receptors are regulated by ovarian steroids in trigeminal ganglia.Methods.—We used reverse transcription‐polymerase chain reaction to examine gene expression in cycling mice, Western blots to examine protein expression, double‐labeling immunohistochemistry using markers of nociceptors and nonnociceptors and confocal microscopy to identify specific types of neurons, and primary tissue culture to examine effects of estrogen on trigeminal neurons in vitro.Results.—In C57/BL6 mice mRNA levels of TPH‐1, the rate‐limiting enzyme in serotonin synthesis, were over 2‐fold higher and protein levels were 1.4‐fold higher at proestrus, the high estrogen stage of the cycle than at diestrus, the low estrogen stage. TPH protein also was present in primary trigeminal cultures obtained from female Sprague‐Dawley rats, but levels were not affected by 24‐hour treatment with physiological levels (10−9 M) of 17β‐estradiol. Gene expression of 5HT‐1B and 5HT‐1D receptors in trigeminal ganglia was not regulated by the estrous cycle. Serotonin was present in trigeminal neurons containing CGRP, a potent vasoactive neuropeptide, peripherin, an intermediate filament present in neurons with unmyelinated axons, neurofilament H, which is present in neurons with myelinated axons, and in neurons binding IB4, a marker of nonpeptidergic nociceptors. Serotonin was also present in neurons containing 5HT‐1B. The serotonin‐positive population was significantly larger in diameter than the serotonin‐negative population.Conclusions.—Expression of the rate‐limiting enzyme required for serotonin synthesis is regulated during the natural estrous cycle, and serotonin is present in larger trigeminal neurons of all the major subtypes. Colocalization of serotonin with 5HT‐1B suggests that this receptor functions as an autoreceptor to regulate serotonin release. Cyclical changes in serotonin levels in trigeminal ganglia could contribute to the pathogenesis of menstrual migraine.

High-Yield Facts Embryology: Early & General Cell Biology: Membranes Cell Biology: Cytoplasm Cell Biology: Intracellular Trafficking Cell Biology: Nucleus Epithelium Connective Tissue Specialized Connective Tissue: Bone and Cartilage Muscle and Cell Motility Nervous System Cardiovascular System, Blood and Bone Marrow Lymphoid System and Cellular Immunology Respiratory System Intergumentary System Gastrointestinal Tract and Glands Endocrine Glands Reproductive Systems Urinary System Eye and Ear Head and Neck Thorax Abdomen Pelvis Extremities Bibliography Index

Hypothyroidism is a common condition. Rarely, it may occur in combination with autoimmune failure of other endocrine glands (autoimmune polyendocrinopathy syndrome type 2, previously known as Schmidt's syndrome). In such cases, restoring normal thyroid function may precipitate adrenal failure. Clinicians should have a high index of suspicion for this condition in patients with Addison's disease, those with a family history of autoimmune endocrine gland failure, patients with one autoimmune endocrine disease who develop nonspecific or serious illness, and patients with type 1 diabetes mellitus whose insulin requirements drop without obvious explanation.

OBJECTIVE:(1) To integrate clinical problem solving into freshman cell and tissue biology (CTB) and (2) to enhance understanding of diabetes using CTB principles to explain the etiology, management, and development of complications in terms of cell, tissue, and organ structure and function.DESCRIPTION:First-year medical students often question the need to learn detailed basic science material. Although clinical content has increased throughout basic science courses, little attempt has been made to link clinical correlations to one another or to enhance use of basic science material in clinical problem solving. The CTB course applies pertinent cell biology concepts such as cell proliferation, differentiation, migration, adhesion, and morphogenesis to tissue and organ function. Diabetes mellitus was chosen as a theme for CTB as diabetes has devastating effects on multiple tissues, and the disease has reached epidemic proportions in the United States, affecting individuals of every age and population group. Type I diabetes, presenting as ketoacidosis in a ten-year-old boy, was introduced by generalist physicians using a "grand rounds" approach. This format challenged students on the first day of medical school to diagnose a patient's problem and to explain the clinical findings in terms of anatomic, biochemical, and physiologic changes. The role of the blood/bicarbonate buffering system was the main focus of faculty-led discussion. The patient was then presented at age 25 with many diabetic complications. This stimulated discussion of the etiology of diabetes (type I versus type II), glycation, and the use of hemoglobin (Hb) A1c to monitor blood sugar control. Compliance and other aspects of diabetes management were added to the discussion. Faculty provided scientific information as necessary, and summary materials were distributed after the sessions. The interaction of a cell biologist with two generalist physicians optimized the integration of basic science with clinical problem solving. During the two semesters of CTB, the diabetes case is frequently referenced. Insulin synthesis provides the model for protein synthesis. Glycation, advanced glycation end products (AGE), and receptors (RAGE) are discussed. Other diabetes-related topics include wound healing (epithelium), basement membrane thickening (connective tissue), insulin regulation of muscle metabolism, diabetic neuropathy (neurohistology), platelet adhesiveness, glycation and HbA1c (blood), osteoporosis and Charcot joints (skeletal system), autoimmune mechanisms (cellular immunology), atherosclerosis and high blood pressure (blood vessels), diabetic nephropathy (renal), altered hepatic and gastrointestinal function, impotence (male reproductive system), and a comparison of type I and type II diabetes (endocrine system).DISCUSSION:Students have provided very positive feedback. The initial case enhanced interest in CTB, established clinical relevance, and has motivated learning and integration of materials from different parts of CTB and other courses. Other courses are now formally linking to the theme. For example, neuroscience will revisit diabetic neuropathy and retinopathy, physiology will relate ketoacidosis to acid-base balance, a human anatomy clinical correlation is being designed for transplantation surgeons to "cure" our diabetic patient with a renal-pancreas transplant. Uses of the case for introduction to clinical medicine, aspects of medical ethics, preventive medicine, and courses in pharmacology and pathology are contemplated.

BACKGROUND:BALB/c mice homozygous for the cpk mutation develop a form of polycystic kidney disease (PKD) with multiorgan pathology similar to human autosomal recessive PKD. Messenger RNA expression in multiple affected organs was analyzed to determine if common gene cascades were misexpressed in the cystic kidney and extrarenal sites of disease. In cystic kidneys, misexpressed mRNAs were found in one of four general groups: proliferation/cell growth, apoptosis, differentiation or extracellular matrix.METHODS:RNA was isolated from kidney, liver and pancreas of cystic and normal BALB/c-cpk mice. Using Northern blot hybridization and ribonuclease protection assays (RPA), the expression of several genes thought to be associated with PKD, namely c-myc, epidermal growth factor receptor (EGF-R) and PKD-1, were evaluated. RPAs were used to assess mRNA expression of cyclins and members of the bax/bcl-2 family. In addition, kidney, liver and pancreas were immunostained for c-Myc and PCNA.RESULTS:Cystic kidney, liver and pancreas all exhibited similar patterns of mRNA misexpression of c-myc, EGF-R and PKD-1. In addition, a number of cell proliferation and apoptosis-related mRNAs also were elevated in cystic kidney and pancreas. Renal epithelial cells expressing proliferation-associated proteins [c-Myc and proliferating cell nuclear antigen (PCNA)] were nearly absent in normal kidney; however, cells of cystic and non-cystic renal tubules plus liver and pancreatic cyst exhibited an increased number of nuclei labeled with antibodies to these proteins.CONCLUSIONS:These data suggest that similar pathologic mechanisms (including the expression of c-myc, EGF-R, PKD-1, cyclin, and bax/bcl-2 family mRNAs) may be responsible for the development of cystic changes in kidney, liver and pancreas in murine autosomal recessive PKD. Treatments targeting these similarly misexpressed mRNAs may be efficacious in ameliorating the cystic pathology in the kidney as well as the other affected organs in ARPKD.

Persons with lactose intolerance are unable to digest significant amounts of lactose because of a genetically inadequate amount of the enzyme lactase. Common symptoms include abdominal pain and bloating, excessive flatus, and watery stool following the ingestion of foods containing lactose. Lactase deficiency is present in up to 15 percent of persons of northern European descent, up to 80 percent of blacks and Latinos, and up to 100 percent of American Indians and Asians. A sizable number of adults believe they are lactose intolerant but do not actually have impaired lactose digestion, and some persons with lactase deficiency can tolerate moderate amounts of ingested lactose. A diagnosis of lactose intolerance can usually be made with a careful history supported by dietary manipulation. If necessary, diagnosis can be confirmed by using a breath hydrogen or lactose tolerance test. Treatment consists primarily of avoiding lactose-containing foods. Lactase enzyme supplements may be helpful. The degree of lactose malabsorption varies greatly among patients with lactose intolerance, but most of them can ingest up to 12 oz of milk daily without symptoms. Lactose-intolerant patients must ensure adequate calcium intake.

Objective: (1) to enhance understanding of CTB using case-based problem solving and simulated patient communication and (2) to stimulate critical thinking and problem-solving skills in a large-scale but interactive format. Description: The goals of the new curriculum at the University of Kansas School of Medicine include integration and application of knowledge, development of critical thinking skills, and an increase in active learning. A typical module in the freshman Cell and Tissue Biology (CTB) course consists of lectures to the class (175 medical students) over basic concepts of an organ/system followed by a “clinical correlation” lecture in which cases are presented. First-year medical students are often overwhelmed with technical terms and lose focused attention during these presentations. Therefore, in 2000 an interactive, problem-solving exercise was developed to engage the class in applying basic concepts to clinical situations. The gastrointestinal module served as the pilot. Clinical and CTB faculty chose celiac disease and lactose intolerance as cases illustrating concepts of cell destruction and metabolic dysfunction, respectively. Case scenarios of symptomatic “patients” were provided, and the students were asked to study the cases and deduce diagnoses before class. The session began in grand-rounds format with clinical faculty leading active deduction of each diagnosis. The students were subsequently divided into about 20 small groups (ten for each of the two disorders) to develop explanations for a newly diagnosed patient. The faculty circulated to coach the groups and distribute a printed synopsis of key aspects of each condition. A role-play was then conducted with a clinical faculty member acting as the patient and randomly selected students as the physician. A brief review followed, emphasizing that understanding CTB aspects of pathologic conditions facilitates diagnosis and is essential to providing adequate explanations to patients. Results of the exercise were evaluated with three questions on the block examination and with student evaluations. Discussion: The session was highly successful in engaging students in the clinical aspects of the gastrointestinal tract, e.g., a 1,300% increase in e-mail questions to the faculty about the topic. The range of discrimination values (comparison of top and bottom 25%) was similar to previous years, but student performance on clinical questions about the gastrointestinal system improved by almost 20%. We also demonstrated that clinicians use CTB material in daily situations to provide patient care. Students reported that the clinical challenge led them to a deeper understanding and appreciation of the CTB material and that it motivated them to study further. These first-year students were surprised that they could successfully apply their knowledge in a clinical situation. The session modeled collaboration between faculty from different departments, and the circulating coaches were particularly effective. All of the students responding to the module evaluation had favorable opinions about the format, with 73.6% strongly agreeing that more of these interactive clinical correlations would be beneficial. The effectiveness of the lecture was rated approximately 25% higher than the effectiveness of other clinical-correlation lectures. The participating faculty enjoyed the experience but thought the session was too short and the class too large for optimum effect. We plan to introduce the same format in other modules and to refine the evaluation techniques.

This title provides medical students as well as physicians with a comprehensive instrument for self-assessment and review within the medical specialty of histology. Each title in the series contains 500 questions designed to parallel the format and degree of difficulty of the questions contained in Step 1 of the USMLE examination. Each question is accompanied by an answer, a paragraph-length explanation and a specific page reference to either a current journal article, a textbook or both. A bibliography lists all sources used, and follows the last chapter of each title within the series.

Annals of the New York Academy of SciencesVolume 752, Issue 1 p. 331-342 Secretion of Plasminogen Activator Activity from Neonatal Rat Heart Cells Is Regulated by Hormones and Growth Factorsa RONAL R. MacGREGOR, RONAL R. MacGREGOR Department of Anatomy and Cell Biology University of Kansas Medical Center Kansas City, Kansas 66160Search for more papers by this authorROBERT M. KLEIN, ROBERT M. KLEIN Department of Anatomy and Cell Biology University of Kansas Medical Center Kansas City, Kansas 66160Search for more papers by this authorDEVI D. BANSAL, DEVI D. BANSAL Department of Anatomy and Cell Biology University of Kansas Medical Center Kansas City, Kansas 66160 Department of Biochemistry Panjab University Chandigarh, IndiaSearch for more papers by this author RONAL R. MacGREGOR, RONAL R. MacGREGOR Department of Anatomy and Cell Biology University of Kansas Medical Center Kansas City, Kansas 66160Search for more papers by this authorROBERT M. KLEIN, ROBERT M. KLEIN Department of Anatomy and Cell Biology University of Kansas Medical Center Kansas City, Kansas 66160Search for more papers by this authorDEVI D. BANSAL, DEVI D. BANSAL Department of Anatomy and Cell Biology University of Kansas Medical Center Kansas City, Kansas 66160 Department of Biochemistry Panjab University Chandigarh, IndiaSearch for more papers by this author First published: March 1995 https://doi.org/10.1111/j.1749-6632.1995.tb17442.xCitations: 4 a Supported by the Kansas Chapter of the American Heart Association. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 Quax, P. H. A., M. Van Den Hoogen, J. H. Verheijen, T. Padro, K. Zehab, T. D. Gelehrter, T. J. C. Van Berkel, J. Kuiper & J. J. Emeis. 1990. Endotoxin induction of plasminogen activator and plasminogen activator inhibitor type I mRNA in rat tissues in vivo. J. Biol. Chem. 265: 15560–15563. 2 Loskutoff, D. J., J. A. Van Mourik, L. A. Erickson & D. Lawrence. 1983. Detection of an unusually stable fibrinolytic inhibitor produced by bovine endothelial cells. Proc. Natl. Acad. Sci. USA 80: 2956–2960. 3 Saksela, O. & D. B. Rifkin. 1988. Cell-associated plasminogen activation: regulation and physiological functions. Annu. Rev. Cell Biol. 4: 93–126. 4 Lyons, R. M., J. Keski-Oja & L. Moses. 1988. Proteolytic activation of latent transforming growth factor-β from fibroblast-conditioned medium. J. Cell Biol. 106: 1659–1665. 5 Saksela, O. & D. B. Rifkin. 1990. Release of basic fibroblast growth factor-heparan sulfate complexes from endothelial cells by plasminogen activator-mediated proteolytic activity. J. Cell. Biol. 110: 767–775. 6 Keski-Oja, J., R. Raghow, M. Sawdey, D. J. Loskutoff, A. E. Postlethwaite, A. H. Kang & H. L. Moses. 1988. Regulation of mRNAs for type-1 plasminogen activator inhibitor, fibronectin, and type I procollagen by transforming growth factor-β. J. Biol. Chem. 263: 3111–3115. 7 Soma, Y. & G. R. Grotendorst. 1989. TGF-β stimulates primary human skin fibroblast DNA synthesis via an autocrine production of PDGF-related peptides. J. Cell Physiol. 140: 246–253. 8 Overall, C. M., J. L. Wrana & J. Sodek. 1989. Independent regulation of collagenase, 72-kDa progelatinase, and metalloendoproteinase inhibitor expression in human fibroblasts by transforming growth factor-β. J. Biol. Chem. 264: 1860–1869. 9 Flaumenhaft, R., M. Abe, P. Mignatti & D. B. Rifkin. 1992. Basic fibroblast growth factor-induced activation of latent transforming growth factor β in endothelial cells: regulation of plasminogen activator activity. J. Cell Biol. 118: 901–909. 10 Flanders, K. C., N. L. Thompson, D. S. Cissel, E. Van Obberghen-Schilling, C. C. Baker, M. E. Kass, L. R. Ellingsworth, A. B. Roberts & M. B. Sporn. 1989. Transforming growth factor-β1: histochemical localization with antibodies to different epitopes. J. Cell Biol. 108: 653–660. 11 Roberts, A. B., N. S. Roche, S. Winokur, J. K. Burmester & M. B. Sporn. 1992. Role of transforming growth factor-β in maintenance of function of cultured cardiac myocytes. J. Clin. Invest. 90: 2056–2062. 12 Brilla, C. G., R. Pick, L. B. Tan, J. S. Janicki & K. T. Weber. 1990. Remodeling of the rat right and left ventricles in experimental hypertension. Circ. Res. 67: 1355–1364. 13 Mayer, M., Z. Finci & M. Chaouat. 1986. Suppression of plasminogen activator activity by dexamethasone in cultured cardiac myocytes. J. Mol. Cell Cardiol. 18: 1117–1124. 14 Bansal, D. D., R. M. Klein & R. R. MacGregor. 1993. Secretion of plasminogen activator from cardiac interstitial cells of SHR and WKY rats. Mol. Biol. Cell 4 (Suppl.): 288A (abstract). 15 Campbell, E. E., M. A. Shitman, J. G. Lewis, J. J. Pasqua & S. V. Pizzo. 1982. A colorimetric assay for releasble plasminogen activator. Clin. Chem. 28: 1125–1128. 16 Bansal, D. D., & R. R. MacGregor. 1990. Secretion of plasminogen activator from bovine parathyroid cells. Endocrinology 126: 2245–2251. 17 Hamilton, J. W., R. R. MacGregor, L. L. H. Chu & D. V. Cohn. 1971. The isolation and partial purification of a non-parathyroid hormone calcemic fraction from bovine parathyroid glands. Endocrinology 89: 1440–1447. 18 Fukuda, Y., Y. Hirata, H. Yoshimi, T. Kojima, Y. Kobayashi, M. Yanagisawa & T. Masaki. 1988. Endothelin is a potent secretagogue for atrial natriuretic peptide in cultured rat atrial myocytes. Biochem. Biophys. Res. Commun. 155: 167–172. 19 Hilal-Dandan, R., K. Urasawa & L. L Brunton. 1992. Endothelin inhibits adenylate cyclase and stimulates phosphoinositide hydrolysis in adult cardiac myocytes. J. Biol. Chem. 267: 10620–10624. 20 Crutchley, D. J., L. B. Conanan & J. R. Maynard. 1981. Human fibroblasts produce inhibitor directed against plasminogen activator when treated with glucocorticoids. Ann. N. Y. Acad. Sci. 370: 609–616. 21 Laiho, M., O. Saksela, P. A. Andreasen & J. Keski-Oja. 1986. Enhanced production and extracellular deposition of the endothelial-type plasminogen activator inhibitor in cultured human lung fibroblasts by transforming growth factor-β. J. Cell. Biol. 103: 2403–2410. Citing Literature Volume752, Issue1Cardiac Growth and RegenerationMarch 1995Pages 331-342 ReferencesRelatedInformation