Search

Your search keyword '"Minrong Ai"' showing total 124 results
Start Over Author "Minrong Ai"
124 results on '"Minrong Ai"'

1. GIP receptor agonism blocks chemotherapy-induced nausea and vomiting

Author

Tito Borner, Benjamin C. Reiner, Richard C. Crist, C. Daniel Furst, Sarah A. Doebley, Julia G. Halas, Minrong Ai, Ricardo J. Samms, Bart C. De Jonghe, and Matthew R. Hayes

Subjects
Incretin, Chemotherapy, Vomiting, Obesity, Diabetes, Antiemetic, Internal medicine, RC31-1245
Abstract

Objective: Nausea and vomiting remain life-threatening obstacles to successful treatment of chronic diseases, despite a cadre of available antiemetic medications. Our inability to effectively control chemotherapy-induced nausea and vomiting (CINV) highlights the need to anatomically, molecularly, and functionally characterize novel neural substrates that block CINV. Methods: Behavioral pharmacology assays of nausea and emesis in 3 different mammalian species were combined with histological and unbiased transcriptomic analyses to investigate the beneficial effects of glucose-dependent insulinotropic polypeptide receptor (GIPR) agonism on CINV. Results: Single-nuclei transcriptomics and histological approaches in rats revealed a topographical, molecularly distinct, GABA-ergic neuronal population in the dorsal vagal complex (DVC) that is modulated by chemotherapy but rescued by GIPR agonism. Activation of DVCGIPR neurons substantially decreased behaviors indicative of malaise in cisplatin-treated rats. Strikingly, GIPR agonism blocks cisplatin-induced emesis in both ferrets and shrews. Conclusion: Our multispecies study defines a peptidergic system that represents a novel therapeutic target for the management of CINV, and potentially other drivers of nausea/emesis.

Published
2023
Full Text
View/download PDF

2. Anorectic and aversive effects of GLP-1 receptor agonism are mediated by brainstem cholecystokinin neurons, and modulated by GIP receptor activation

Author

Alessia Costa, Minrong Ai, Nicolas Nunn, Isabella Culotta, Jenna Hunter, Mehdi Boutagouga Boudjadja, Lourdes Valencia-Torres, Gabriella Aviello, David J. Hodson, Brandy M. Snider, Tamer Coskun, Paul J. Emmerson, Simon M. Luckman, and Giuseppe D'Agostino

Subjects
Brain, Appetite, Nausea, Glucagon-like peptide-1, Glucose-dependent insulinotropic polypeptide, Cholecystokinin, Internal medicine, RC31-1245
Abstract

Objective: Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are effective medications to reduce appetite and body weight. These actions are centrally mediated; however, the neuronal substrates involved are poorly understood. Methods: We employed a combination of neuroanatomical, genetic, and behavioral approaches in the mouse to investigate the involvement of caudal brainstem cholecystokinin-expressing neurons in the effect of the GLP-1RA exendin-4. We further confirmed key neuroanatomical findings in the non-human primate brain. Results: We found that cholecystokinin-expressing neurons in the caudal brainstem are required for the anorectic and body weight-lowering effects of GLP-1RAs and for the induction of GLP-1RA-induced conditioned taste avoidance. We further show that, while cholecystokinin-expressing neurons are not a direct target for glucose-dependent insulinotropic peptide (GIP), GIP receptor activation results in a reduced recruitment of these GLP-1RA-responsive neurons and a selective reduction of conditioned taste avoidance. Conclusions: In addition to disclosing a neuronal population required for the full appetite- and body weight-lowering effect of GLP-1RAs, our data also provide a novel framework for understanding and ameliorating GLP-1RA-induced nausea — a major factor for withdrawal from treatment.

Published
2022
Full Text
View/download PDF

3. Green-to-Red Photoconversion of GCaMP.

Author

Minrong Ai, Holly Mills, Makoto Kanai, Jason Lai, Jingjing Deng, Eric Schreiter, Loren Looger, Thomas Neubert, and Greg Suh

Subjects
Medicine, Science
Abstract

Genetically encoded calcium indicators (GECIs) permit imaging intracellular calcium transients. Among GECIs, the GFP-based GCaMPs are the most widely used because of their high sensitivity and rapid response to changes in intracellular calcium concentrations. Here we report that the fluorescence of GCaMPs--including GCaMP3, GCaMP5 and GCaMP6--can be converted from green to red following exposure to blue-green light (450-500 nm). This photoconversion occurs in both insect and mammalian cells and is enhanced in a low oxygen environment. The red fluorescent GCaMPs retained calcium responsiveness, albeit with reduced sensitivity. We identified several amino acid residues in GCaMP important for photoconversion and generated a GCaMP variant with increased photoconversion efficiency in cell culture. This light-induced spectral shift allows the ready labeling of specific, targeted sets of GCaMP-expressing cells for functional imaging in the red channel. Together, these findings indicate the potential for greater utility of existing GCaMP reagents, including transgenic animals.

Published
2015
Full Text
View/download PDF

4. Anti-lubricin monoclonal antibodies created using lubricin-knockout mice immunodetect lubricin in several species and in patients with healthy and diseased joints.

Author

Minrong Ai, Yajun Cui, Man-Sun Sy, David M Lee, Ling Xiu Zhang, Katherine M Larson, Kyle C Kurek, Gregory D Jay, and Matthew L Warman

Subjects
Medicine, Science
Abstract

Lubricin, encoded by the gene PRG4, is the principal lubricant in articulating joints. We immunized mice genetically deficient for lubricin (Prg4-/-) with purified human lubricin, and generated several mAbs. We determined each mAb's binding epitope, sensitivity, and specificity using biologic samples and recombinant lubricin sub-domains, and we also developed a competition ELISA assay to measure lubricin in synovial fluid and blood. We found the mAbs all recognized epitopes containing O-linked oligosaccharides conjugated to the peptide motif KEPAPTTT. By western blot, the mAbs detected lubricin in 1 μl of synovial fluid from several animal species, including human. The mAbs were specific for lubricin since they did not cross-react with other synovial fluid constituents from patients with camptodactyly-arthropathy-coxa vara-pericarditis syndrome (CACP), who genetically lack this protein. The competition ELISA detected lubricin in blood samples from healthy individuals but not from patients with CACP, indicating blood can be used in a diagnostic test for patients suspected of having CACP. Lubricin epitopes in blood do not represent degradation fragments from synovial fluid. Therefore, although blood lubricin levels did not differentiate patients with inflammatory joint disease from healthy controls, epitope-specific anti-lubricin mAbs could be useful for monitoring disease activity in synovial fluid.

Published
2015
Full Text
View/download PDF

5. GIP Receptor Agonism Attenuates GLP-1 Receptor Agonist–Induced Nausea and Emesis in Preclinical Models

Author

Jorge Alsina-Fernandez, Matthew R. Hayes, Arianna White, Ricardo J. Samms, Benjamin C. Reiner, Misgana Y. Ghidewon, Ankur Bamezai, Mridula Dogra, Samantha M. Fortin, Tito Borner, Caroline E. Geisler, Harvey J. Grill, Richard Cosgrove, Richard C. Crist, Jane Gaisinsky, Marcos J. Sanchez-Navarro, Sarah A. Doebley, Bart C. De Jonghe, Minrong Ai, and Rosa M Leon

Subjects
Male, Vomiting, Nausea, Endocrinology, Diabetes and Metabolism, Pharmacology, Inhibitory postsynaptic potential, Glucagon-Like Peptide-1 Receptor, Receptors, Gastrointestinal Hormone, Rats, Sprague-Dawley, Mice, Diabetes mellitus, Internal Medicine, medicine, Animals, Receptor, Glucagon-like peptide 1 receptor, business.industry, Shrews, Body Weight, digestive, oral, and skin physiology, Area postrema, Feeding Behavior, medicine.disease, Rats, Mice, Inbred C57BL, nervous system, GABAergic, medicine.symptom, business, hormones, hormone substitutes, and hormone antagonists
Abstract

Glucagon-like peptide 1 receptor (GLP-1R) agonists decrease body weight and improve glycemic control in obesity and diabetes. Patient compliance and maximal efficacy of GLP-1 therapeutics are limited by adverse side effects, including nausea and emesis. In three different species (i.e., mice, rats, and musk shrews), we show that glucose-dependent insulinotropic polypeptide receptor (GIPR) signaling blocks emesis and attenuates illness behaviors elicited by GLP-1R activation, while maintaining reduced food intake, body weight loss, and improved glucose tolerance. The area postrema and nucleus tractus solitarius (AP/NTS) of the hindbrain are required for food intake and body weight suppression by GLP-1R ligands and processing of emetic stimuli. Using single-nuclei RNA sequencing, we identified the cellular phenotypes of AP/NTS cells expressing GIPR and GLP-1R on distinct populations of inhibitory and excitatory neurons, with the greatest expression of GIPR in γ-aminobutyric acid-ergic neurons. This work suggests that combinatorial pharmaceutical targeting of GLP-1R and GIPR will increase efficacy in treating obesity and diabetes by reducing nausea and vomiting.

Published
2021

6. Anorectic and aversive effects of GLP-1 receptor agonism are mediated by brainstem cholecystokinin neurons, and modulated by GIP receptor activation

Author

Paul J. Emmerson, David J. Hodson, Brandy M. Snider, Nicolas Nunn, Tamer Coskun, Jenna Hunter, Mehdi Boutagouga Boudjadja, Gabriella Aviello, Isabella Culotta, Minrong Ai, Simon M. Luckman, Alessia Costa, Giuseppe D'Agostino, Lourdes Valencia-Torres, Costa, A., Ai, M., Nunn, N., Culotta, I., Hunter, J., Boudjadja, M. B., Valencia-Torres, L., Aviello, G., Hodson, D. J., Snider, B. M., Coskun, T., Emmerson, P. J., Luckman, S. M., and D'Agostino, G.

Subjects
Blood Glucose, Male, Glucagon-like peptide-1, endocrine system, Glucose-dependent insulinotropic polypeptide, media_common.quotation_subject, Appetite, Gastric Inhibitory Polypeptide, Brief Communication, Glucagon-Like Peptide-1 Receptor, Receptors, Gastrointestinal Hormone, Mice, Nucleus of the solitary tract, Glucagon-Like Peptide 1, Appetite Depressants, Medicine, Animals, Hypoglycemic Agents, Insulin, Receptor, Internal medicine, Molecular Biology, Glucagon-like peptide 1 receptor, media_common, Cholecystokinin, Neurons, business.industry, Area postrema, digestive, oral, and skin physiology, Brain, Nausea, Cell Biology, Liraglutide, Glucagon, RC31-1245, Mice, Inbred C57BL, Anorectic, Exenatide, Female, Brainstem, business, Neuroscience, hormones, hormone substitutes, and hormone antagonists
Abstract

Objective Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are effective medications to reduce appetite and body weight. These actions are centrally mediated; however, the neuronal substrates involved are poorly understood. Methods We employed a combination of neuroanatomical, genetic, and behavioral approaches in the mouse to investigate the involvement of caudal brainstem cholecystokinin-expressing neurons in the effect of the GLP-1RA exendin-4. We further confirmed key neuroanatomical findings in the non-human primate brain. Results We found that cholecystokinin-expressing neurons in the caudal brainstem are required for the anorectic and body weight-lowering effects of GLP-1RAs and for the induction of GLP-1RA-induced conditioned taste avoidance. We further show that, while cholecystokinin-expressing neurons are not a direct target for glucose-dependent insulinotropic peptide (GIP), GIP receptor activation results in a reduced recruitment of these GLP-1RA-responsive neurons and a selective reduction of conditioned taste avoidance. Conclusions In addition to disclosing a neuronal population required for the full appetite- and body weight-lowering effect of GLP-1RAs, our data also provide a novel framework for understanding and ameliorating GLP-1RA-induced nausea — a major factor for withdrawal from treatment., Highlights • CCKAP/NTS neurons are required for the full anorectic and body weight-lowering effect of GLP-1 receptor agonists. • GLP-1 receptor agonists promote the formation of conditioned taste avoidance by activating CCKAP/NTS neurons. • CCKAP/NTS neurons are not activated in response to GIP receptor agonists. • GIP receptor agonists reduce GLP-1 receptor agonist-induced neuronal responses in the caudal brainstem. • GIP receptor agonists reduce GLP-1 receptor agonist-induced conditioned taste avoidance.

Published
2021

7. GIPR Agonism Inhibits PYY-Induced Nausea-Like Behavior

Author

Ricardo J. Samms, Richard Cosgrove, Brandy M. Snider, Ellen C. Furber, Brian A. Droz, Daniel A. Briere, James Dunbar, Mridula Dogra, Jorge Alsina-Fernandez, Tito Borner, Bart C. De Jonghe, Matthew R. Hayes, Tamer Coskun, Kyle W. Sloop, Paul J. Emmerson, and Minrong Ai

Subjects
Mice, Endocrinology, Diabetes and Metabolism, Internal Medicine, Animals, Nausea, Peptide YY, Anti-Obesity Agents, Obesity, Receptors, Gastrointestinal Hormone
Abstract

The induction of nausea and emesis is a major barrier to maximizing the weight loss profile of obesity medications, and therefore, identifying mechanisms that improve tolerability could result in added therapeutic benefit. The development of Peptide YY (PYY)-based approaches to treat obesity are no exception, as PYY receptor agonism is often accompanied by nausea and vomiting. Here, we sought to determine whether glucose-dependent insulinotropic polypeptide (GIP) receptor agonism reduces PYY-induced nausea-like behavior in mice. We found that central and peripheral administration of a GIPR agonist (GIPRA) reduced conditioned taste avoidance (CTA) without affecting hypophagia mediated by a PYY analog. The receptors for GIP and PYY (Gipr and Npy2r) were found to be expressed by the same neurons in the area postrema (AP), a brainstem nucleus involved in detecting aversive stimuli. Peripheral administration of a GIPRA induced neuronal activation (cFos) in the AP. Further, whole-brain cFos analyses indicated that PYY-induced CTA was associated with augmented neuronal activity in the parabrachial nucleus (PBN), a brainstem nucleus that relays aversive/emetic signals to brain regions that control feeding behavior. Importantly, GIPR agonism reduced PYY-mediated neuronal activity in the PBN, providing a potential mechanistic explanation for how GIPRA treatment reduces PYY-induced nausea-like behavior. Together, our study provides a novel mechanism by which GIP-based therapeutics may benefit the tolerability of weight loss agents.

Published
2021

8. GIP Receptor Agonism Attenuates GLP-1 Receptor Agonist Induced Nausea and Emesis in Preclinical Models

Author

Matthew R. Hayes, Bart C. De Jonghe, Ricardo J. Samms, Minrong Ai, Benjamin C. Reiner, Richard C. Crist, Harvey J. Grill, Misgana Y. Ghidewon, Ankur Bamezai, Arianna White, Jane Gaisinsky, Rosa M. Leon, Marcos J. Sanchez-Navarro, Sarah Doebley, Mridula Dogra, Jorge Alsina-Fernandez, Richard Cosgrove, Samantha M. Fortin, Caroline E. Geisler, and Tito Borner

Subjects
nervous system, digestive, oral, and skin physiology
Abstract

Glucagon-like peptide-1 receptor (GLP-1R) agonists decrease body weight and improve glycemic control in obesity and diabetes. Patient compliance and maximal efficacy of GLP-1 therapeutics are limited by side effects including nausea and emesis. In three different species (i.e., mice, rats, and musk shrews), we show that glucose-dependent insulinotropic polypeptide receptor (GIPR) signaling blocks emesis and attenuates illness behaviors elicited by GLP-1R activation, while maintaining reduced food intake, body weight loss, and improved glucose tolerance. The area postrema and nucleus tractus solitarius (AP/NTS) of the hindbrain are required for food intake and body weight suppression by GLP-1R ligands and processing of emetic stimuli. Utilizing single-nuclei RNA-sequencing, we identified the cellular phenotypes of AP/NTS GIPR- and GLP-1R-expressing cells on distinct populations of inhibitory and excitatory neurons, with the greatest expression of GIPR in GABAergic neurons. This work suggests that combinatorial pharmaceutical targeting of GLP-1R and GIPR will increase efficacy in treating obesity and diabetes by reducing nausea and vomiting.

Published
2021

9. Long-Acting and Selective Oxytocin Peptide Analogs Show Antidiabetic and Antiobesity Effects in Male Mice

Author

Andrew C. Adams, Jill A. Willency, Qian Yang, Keyun Qing, Xiaojun Wang, Minrong Ai, Alexander M. Efanov, Xiao-peng Yu, Andrea Renee Geiser, Paul J. Emmerson, Jianliang Lu, Jorge Alsina-Fernandez, Tamer Coskun, Brandy M. Snider, Emily C Beebe, and Lili Guo

Subjects
0301 basic medicine, medicine.medical_specialty, Vasopressin, Diabetes, Pancreatic and Gastrointestinal Hormones, vasopressin, Endocrinology, Diabetes and Metabolism, media_common.quotation_subject, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, oxytocin, acylation, medicine, Receptor, Research Articles, Vasopressin receptor, media_common, Peptide analog, Chemistry, Glucagon secretion, Appetite, Oxytocin receptor, 030104 developmental biology, Endocrinology, Oxytocin, weight loss, hormones, hormone substitutes, and hormone antagonists, 030217 neurology & neurosurgery, medicine.drug
Abstract

Oxytocin (OXT) has been shown to suppress appetite, induce weight loss, and improve glycemic control and lipid metabolism in several species, including humans, monkeys, and rodents. However, OXT’s short half-life in circulation and lack of receptor selectivity limit its application and efficacy. In this study, we report an OXT peptide analog (OXTGly) that is potent and selective for the OXT receptor (OXTR). OXT, but not OXTGly, activated vasopressin receptors in vitro and acutely increased blood pressure in vivo when administered IP. OXT suppressed food intake in mice, whereas OXTGly had a moderate effect on food intake when administered IP or intracerebroventricularly. Both OXT (IP) and OXTGly (IP) improved glycemic control in glucose tolerance tests. Additionally, both OXT (IP) and OXTGly (IP) stimulated insulin, glucagon-like peptide 1, and glucagon secretion in mice. We generated lipid-conjugated OXT (acylated-OXT) and OXTGly (acylated-OXTGly) and demonstrated that these molecules have significantly extended half-lives in vivo. Compared with OXT, 2-week treatment of diet-induced obese mice with acylated-OXT [subcutaneous(ly) (SC)] resulted in enhanced body weight reduction, an improved lipid profile, and gene expression changes consistent with increased lipolysis and decreased gluconeogenesis. Treatment with acylated-OXTGly (SC) also resulted in a statistically significant weight loss, albeit to a lesser degree compared with acylated-OXT treatment. In conclusion, we demonstrate that selective activation of the OXTR pathway results in both acute and chronic metabolic benefits, whereas potential activation of vasopressin receptors by nonselective OXT analogs causes physiological stress that contributes to additional weight loss.

Published
2019

10. A mutation in the signal sequence ofLRP5in a family with an osteoporosis-pseudoglioma syndrome (OPPG)-like phenotype indicates a novel disease mechanism for trinucleotide repeats

Author

Minrong Ai, Cynthia F. Bartels, Stefan Höning, Christian Kubisch, Oya Uyguner, Christian Netzer, Alfredo Ramirez, Franz-Georg Hanisch, Bernd Wollnik, Hülya Kayserili, Abdullah Uzumcu, Matthew L. Warman, Peter Nürnberg, Jan Freudenberg, Gudrun Nürnberg, and Boi-Dinh Chung

Subjects
Male, Signal peptide, Eye Diseases, Genotype, Turkey, Recombinant Fusion Proteins, Blotting, Western, Population, Alu element, Protein Sorting Signals, Biology, medicine.disease_cause, Cell Line, Gene Frequency, Trinucleotide Repeats, Leucine, Genetics, medicine, Humans, Abnormalities, Multiple, Amino Acid Sequence, Luciferases, education, Allele frequency, Peptide sequence, LDL-Receptor Related Proteins, Genetics (clinical), Family Health, Mutation, education.field_of_study, Base Sequence, Syndrome, Molecular biology, Pedigree, Low Density Lipoprotein Receptor-Related Protein-5, Dynamic mutation, Osteoporosis, Female, Trinucleotide repeat expansion
Abstract

We extend the spectrum of phenotypes caused by mutations in the Wnt/Norrin coreceptor low-density lipoprotein receptor-related protein 5 (LRP5) by identifying two novel types of mutation in related individuals whose presenting features were profound muscle hypotonia, mild mental retardation, blindness, and growth retardation. One mutation removes 6 out of 9 consecutive leucine residues in the LRP5 signal peptide (c.43_60del or p.Leu15_Leu20del), which impairs polypeptide entry into the endoplasmic reticulum (ER), trafficking to the cell membrane, and signal transduction. The second mutation resulted from nonhomologous recombination between Alu repeat sequences, which deleted exons 14-16 and would produce a nonfunctional, truncated, and frameshifted polypeptide, if expressed [chr11:g.(13871447_1387511)_(13879636_13879700)del (NW_925106.1) or p.Pro1010GlnfsX38]. We confirmed that the length of the LRP5 signal peptide poly-leucine repeat is polymorphic in the general population, and, importantly, we were able to demonstrate in independent in vitro assays that different allele sizes affect receptor processing and signal transduction. Consequently, this polymorphism may have physiologic effects in vivo. This latter finding is relevant since through a genomewide search we identified nearly 400 human proteins that contain poly-leucine repeats within their signal peptide. We chose 18 of these proteins and genotyped the underlying trinucleotide repeat in healthy Caucasian individuals. More than one length allele was observed in one-half of the proteins. We therefore propose that natural variation in poly-leucine-stretches within signal peptides constitutes a currently unrecognized source of variability in protein translation and expression.

Published
2009

11. Green-to-Red Photoconversion of GCaMP

Author

Holly Mills, Jason Sih-Yu Lai, Minrong Ai, Greg S. B. Suh, Jingjing Deng, Loren L. Looger, Makoto I. Kanai, Eric R. Schreiter, and Thomas A. Neubert

Subjects
Fluorescence-lifetime imaging microscopy, Recombinant Fusion Proteins, Green Fluorescent Proteins, Color, chemistry.chemical_element, lcsh:Medicine, Calcium, Biology, Fluorescence, Calcium in biology, Green fluorescent protein, Animals, Genetically Modified, Calcium imaging, Calmodulin, Fluorescence microscope, Animals, Humans, lcsh:Science, Myosin-Light-Chain Kinase, Multidisciplinary, lcsh:R, Photochemical Processes, Peptide Fragments, Drosophila melanogaster, HEK293 Cells, chemistry, Biochemistry, GCaMP, Biophysics, lcsh:Q, Research Article
Abstract

Genetically encoded calcium indicators (GECIs) permit imaging intracellular calcium transients. Among GECIs, the GFP-based GCaMPs are the most widely used because of their high sensitivity and rapid response to changes in intracellular calcium concentrations. Here we report that the fluorescence of GCaMPs--including GCaMP3, GCaMP5 and GCaMP6--can be converted from green to red following exposure to blue-green light (450-500 nm). This photoconversion occurs in both insect and mammalian cells and is enhanced in a low oxygen environment. The red fluorescent GCaMPs retained calcium responsiveness, albeit with reduced sensitivity. We identified several amino acid residues in GCaMP important for photoconversion and generated a GCaMP variant with increased photoconversion efficiency in cell culture. This light-induced spectral shift allows the ready labeling of specific, targeted sets of GCaMP-expressing cells for functional imaging in the red channel. Together, these findings indicate the potential for greater utility of existing GCaMP reagents, including transgenic animals.

Published
2015

12. Anti-lubricin monoclonal antibodies created using lubricin-knockout mice immunodetect lubricin in several species and in patients with healthy and diseased joints

Author

Kyle C. Kurek, Gregory D. Jay, Yajun Cui, Matthew L. Warman, Man Sun Sy, Ling Xiu Zhang, Minrong Ai, Katherine M. Larson, and David M. Lee

Subjects
Coxa Vara, Male, Oligosaccharides, lcsh:Medicine, Epitope, law.invention, Epitopes, Mice, 0302 clinical medicine, law, Antibody Specificity, Blood plasma, Synovial Fluid, lcsh:Science, Mice, Knockout, 0303 health sciences, Multidisciplinary, Synovitis, biology, medicine.diagnostic_test, Antibodies, Monoclonal, Middle Aged, 3. Good health, Recombinant DNA, Female, Antibody, Arthropathy, Neurogenic, Hand Deformities, Congenital, Oligopeptides, Research Article, Adult, medicine.drug_class, Enzyme-Linked Immunosorbent Assay, Monoclonal antibody, 03 medical and health sciences, Western blot, medicine, Synovial fluid, Animals, Humans, Amino Acid Sequence, 030304 developmental biology, Aged, Glycoproteins, 030203 arthritis & rheumatology, business.industry, lcsh:R, medicine.disease, Molecular biology, Case-Control Studies, Immunology, biology.protein, Joints, lcsh:Q, business
Abstract

Lubricin, encoded by the gene PRG4, is the principal lubricant in articulating joints. We immunized mice genetically deficient for lubricin (Prg4-/-) with purified human lubricin, and generated several mAbs. We determined each mAb’s binding epitope, sensitivity, and specificity using biologic samples and recombinant lubricin sub-domains, and we also developed a competition ELISA assay to measure lubricin in synovial fluid and blood. We found the mAbs all recognized epitopes containing O-linked oligosaccharides conjugated to the peptide motif KEPAPTTT. By western blot, the mAbs detected lubricin in 1 μl of synovial fluid from several animal species, including human. The mAbs were specific for lubricin since they did not cross-react with other synovial fluid constituents from patients with camptodactyly-arthropathy-coxa vara-pericarditis syndrome (CACP), who genetically lack this protein. The competition ELISA detected lubricin in blood samples from healthy individuals but not from patients with CACP, indicating blood can be used in a diagnostic test for patients suspected of having CACP. Lubricin epitopes in blood do not represent degradation fragments from synovial fluid. Therefore, although blood lubricin levels did not differentiate patients with inflammatory joint disease from healthy controls, epitope-specific anti-lubricin mAbs could be useful for monitoring disease activity in synovial fluid.

Published
2015

13. Clinical and Molecular Findings in Osteoporosis-Pseudoglioma Syndrome

Author

Cynthia F. Bartels, Deborah K. Schelling, Shauna Heeger, and Minrong Ai

Subjects
Proband, medicine.medical_specialty, FZD4, Mutation, Missense, Consanguinity, Biology, medicine.disease_cause, Bone Density, Locus heterogeneity, Internal medicine, Genetics, medicine, Missense mutation, Abnormalities, Multiple, Genetics(clinical), Eye Abnormalities, Allele, LDL-Receptor Related Proteins, Genetics (clinical), Mutation, LRP5, Syndrome, Articles, medicine.disease, Wnt Proteins, Low Density Lipoprotein Receptor-Related Protein-5, Endocrinology, Osteoporosis
Abstract

Mutations in the low-density lipoprotein receptor–related protein 5 gene (LRP5) cause autosomal recessive osteoporosis-pseudoglioma syndrome (OPPG). We sequenced the coding exons of LRP5 in 37 probands suspected of having OPPG on the basis of the co-occurrence of severe congenital or childhood-onset visual impairment with bone fragility or osteoporosis recognized by young adulthood. We found two putative mutant alleles in 26 probands, only one mutant allele in 4 probands, and no mutant alleles in 7 probands. Looking for digenic inheritance, we sequenced the genes encoding the functionally related receptor LRP6, an LRP5 coreceptor FZD4, and an LRP5 ligand, NDP, in the four probands with one mutant allele, and, looking for locus heterogeneity, we sequenced FZD4 and NDP in the seven probands with no mutations, but we found no additional mutations. When we compared clinical features between probands with and without LRP5 mutations, we found no difference in the severity of skeletal disease, prevalence of cognitive impairment, or family history of consanguinity. However, four of the seven probands without detectable mutations had eye pathology that differed from pathology previously described for OPPG. Since many LRP5 mutations are missense changes, to differentiate between a disease-causing mutation and a benign variant, we measured the ability of wild-type and mutant LRP5 to transduce Wnt and Norrin signal ex vivo. Each of the seven OPPG mutations tested, had reduced signal transduction compared with wild-type mutations. These results indicate that early bilateral vitreoretinal eye pathology coupled with skeletal fragility is a strong predictor of LRP5 mutation and that mutations in LRP5 cause OPPG by impairing Wnt and Norrin signal transduction.

Published
2005

14. Reduced Affinity to and Inhibition by DKK1 Form a Common Mechanism by Which High Bone Mass-Associated Missense Mutations in LRP5 Affect Canonical Wnt Signaling

Author

Matthew L. Warman, Minrong Ai, Sheri L. Holmen, Wim Van Hul, and Bart O. Williams

Subjects
Models, Molecular, Mutant, Mutation, Missense, Wnt1 Protein, Biology, Animals, Humans, Missense mutation, Receptor, Molecular Biology, LDL-Receptor Related Proteins, Wnt signaling pathway, Proteins, LRP5, Cell Biology, Molecular biology, Protein Structure, Tertiary, Wnt Proteins, Low Density Lipoprotein Receptor-Related Protein-5, Phenotype, DKK1, Intercellular Signaling Peptides and Proteins, Bone Diseases, Signal transduction, WNT3A, Molecular Chaperones, Signal Transduction
Abstract

The low-density-lipoprotein receptor-related protein 5 (LRP5), a coreceptor in the canonical Wnt signaling pathway, has been implicated in human disorders of low and high bone mass. Loss-of-function mutations cause the autosomal recessive osteoporosis-pseudoglioma syndrome, and heterozygous missense mutations in families segregating autosomal dominant high bone mass (HBM) phenotypes have been identified. We expressed seven different HBM-LRP5 missense mutations to delineate the mechanism by which they alter Wnt signaling. None of the mutations caused activation of the receptor in the absence of ligand. Each mutant receptor was able to reach the cell surface, albeit at differing amounts, and transduce exogenously supplied Wnt1 and Wnt3a signal. All HBM mutant proteins had reduced physical interaction with and reduced inhibition by DKK1. These data suggest that HBM mutant proteins can transit to the cell surface in sufficient quantity to transduce Wnt signal and that the likely mechanism for the HBM mutations' physiologic effects is via reduced affinity to and inhibition by DKK1.

Published
2005

15. Taste-independent nutrient selection is mediated by a brain-specific Na+/solute cotransporter in Drosophila

Author

Monica Dus, Greg S. B. Suh, and Minrong Ai

Subjects
Taste, Sodium, CD8 Antigens, Green Fluorescent Proteins, chemistry.chemical_element, Receptors, Cell Surface, Choice Behavior, Sodium-Glucose Transport Proteins, Article, Animals, Genetically Modified, Food Preferences, Nutrient, Hemolymph, Animals, Drosophila Proteins, Humans, Sugar, Drosophila, Neurons, Analysis of Variance, biology, Base Sequence, Dose-Response Relationship, Drug, General Neuroscience, fungi, Brain, Transporter, biology.organism_classification, Glucose, Biochemistry, chemistry, Gene Expression Regulation, Mutation, RNA Interference, Food Deprivation, Glycogen, Transcription Factors
Abstract

Animals can determine the nutritional value of sugar without the influence of taste. Here, we describe a Drosophila mutant that is insensitive to the nutritional value of sugars, but responds only to the concentration (i.e. sweetness). The affected gene encodes a sodium/solute cotransporter-like protein, designated dSLC5A11 (or cupcake), which is structurally similar to mammalian sodium/glucose cotransporters (SGLTs) that transport sugar across the intestinal and renal lumen. However, dSLC5A11 is prominently expressed in 10-13 pairs of R4 neurons of the ellipsoid body (EB) in the brain and functions in these neurons for selecting appropriate foods. We propose that dSLC5A11 and EB R4 neurons carry out a critical signaling function in responding to internal glycemic levels.

Published
2013

16. Decreased BMD and Limb Deformities in Mice Carrying Mutations in Both Lrp5 and Lrp6

Author

Sheri L. Holmen, Minrong Ai, Matthew L. Warman, Cassandra R. Zylstra, Bree D. Buckner-Berghuis, Mary L. Bouxsein, Troy A. Giambernardi, J. Fred Hess, Bart O. Williams, James H. Resau, and Vaida Glatt

Subjects
Male, Heterozygote, medicine.medical_specialty, Time Factors, Genotype, Endocrinology, Diabetes and Metabolism, Osteoporosis, Limb Deformities, Congenital, Mice, Transgenic, Biology, Ligands, medicine.disease_cause, Loss of heterozygosity, Mice, Sex Factors, Bone Density, Internal medicine, medicine, Animals, Humans, Limb development, Orthopedics and Sports Medicine, LDL-Receptor Related Proteins, Mice, Knockout, Mutation, Dose-Response Relationship, Drug, Microcirculation, Homozygote, LRP6, Extremities, LRP5, medicine.disease, Penetrance, Wnt Proteins, Low Density Lipoprotein Receptor-Related Protein-5, Phenotype, Endocrinology, Receptors, LDL, Low Density Lipoprotein Receptor-Related Protein-6, Knockout mouse, Intercellular Signaling Peptides and Proteins, Female, Tomography, X-Ray Computed, Protein Binding
Abstract

Humans and mice lacking Lrp5 have low BMD. To evaluate whether Lrp5 and Lrp6 interact genetically to control bone or skeletal development, we created mice carrying mutations in both Lrp5 and the related gene Lrp6. We found that compound mutants had dose-dependent deficits in BMD and limb formation, suggesting functional redundancy between these two genes in bone and limb development. Introduction: Lrp5 and Lrp6 are closely related members of the low density lipoprotein receptor family and are co-receptors for Wnt ligands. While Lrp5 mutations are associated with low BMD in humans and mice, the role of Lrp6 in bone formation has not been analyzed. Materials and Methods: To address whether Lrp5 and Lrp6 play complimentary roles in bone and skeletal development, we created mice with mutations in both genes. We inspected limbs of mice from the different genotypic classes of compound mutants to identify abnormalities. DXA and CT were used to evaluate the effect of mutations in Lrp5 and Lrp6 on BMD and microarchitecture. Results: Mice heterozygous for mutations in Lrp6 and either heterozygous or homozygous for a mutation in Lrp5 (Lrp6 / ;Lrp5 / or Lrp6 / ;Lrp5 / ) display limb defects with incomplete penetrance and variable expression. DXA analysis showed that BMD decreased as mice progressively were more deficient in Lrp5 and Lrp6. Lrp6 / ; Lrp5 / mice were more severely affected than Lrp6 / ;Lrp5 / mice, whereas Lrp6 / ;Lrp5 / mice had statistically higher BMD than Lrp6 / ;Lrp5 / mice and lower BMD compared with wildtype mice and mice heterozygous for either mutation alone. Conclusions: Lrp6 and Lrp5 genetically interact in limb development in mice. Furthermore, heterozygosity for an inactivating mutation in Lrp6 further reduces BMD in both male and female mice lacking Lrp5. J Bone Miner Res 2004;19:2033-2040. Published online on Sepember 13, 2004; doi: 10.1359/JBMR.040907

Published
2004

17. Ionotropic glutamate receptors IR64a and IR8a form a functional odorant receptor complex in vivo in Drosophila

Author

Jin-Yong Park, Greg S. B. Suh, Steven Blais, Thomas A. Neubert, Soohong Min, and Minrong Ai

Subjects
DNA, Complementary, Protein subunit, Xenopus, Blotting, Western, Green Fluorescent Proteins, Sensory system, Biology, Receptors, Ionotropic Glutamate, Ion Channels, Olfactory Receptor Neurons, Animals, Genetically Modified, medicine, Animals, Drosophila Proteins, Immunoprecipitation, Receptor, Olfactory receptor, Behavior, Animal, General Neuroscience, Glutamate receptor, Articles, Immunohistochemistry, Cell biology, Smell, medicine.anatomical_structure, Biochemistry, Oocytes, Antennal lobe, Calcium, Drosophila, Ion Channel Gating, Drosophila Protein, Ionotropic effect
Abstract

Drosophila olfactory sensory neurons express either odorant receptors or ionotropic glutamate receptors (IRs). The sensory neurons that express IR64a, a member of the IR family, send axonal projections to either the DC4 or DP1m glomeruli in the antennal lobe. DC4 neurons respond specifically to acids/protons, whereas DP1m neurons respond to a broad spectrum of odorants. The molecular composition of IR64a-containing receptor complexes in either DC4 or DP1m neurons is not known, however. Here, we immunoprecipitated the IR64a protein from lysates of fly antennal tissue and identified IR8a as a receptor subunit physically associated with IR64a by mass spectrometry. IR8a mutants and flies in which IR8a was knocked down by RNAi in IR64a+ neurons exhibited defects in acid-evoked physiological and behavioral responses. Furthermore, we found that the loss of IR8a caused a significant reduction in IR64a protein levels. When expressed in Xenopus oocytes, IR64a and IR8a formed a functional ion channel that allowed ligand-evoked cation currents. These findings provide direct evidence that IR8a is a subunit that forms a functional olfactory receptor with IR64a in vivo to mediate odor detection.

Published
2013

18. Dedicated olfactory neurons mediating attraction behavior to ammonia and amines in Drosophila

Author

Greg S. B. Suh, Minrong Ai, Soohong Min, and Seul A Shin

Subjects
Population, Sensory system, Receptors, Ionotropic Glutamate, Olfactory Receptor Neurons, Animals, Genetically Modified, Species Specificity, Ammonia, Anopheles, medicine, Animals, Amines, Receptor, education, Drosophila, Afferent Pathways, Analysis of Variance, education.field_of_study, Multidisciplinary, biology, Chemotaxis, biology.organism_classification, Immunohistochemistry, Attraction, Smell, medicine.anatomical_structure, nervous system, PNAS Plus, Antennal lobe, Drosophila melanogaster, Neuroscience
Abstract

Animals across various phyla exhibit odor-evoked innate attraction behavior that is developmentally programmed. The mechanism underlying such behavior remains unclear because the odorants that elicit robust attraction responses and the neuronal circuits that mediate this behavior have not been identified. Here, we describe a functionally segregated population of olfactory sensory neurons (OSNs) and projection neurons (PNs) in Drosophila melanogaster that are highly specific to ammonia and amines, which act as potent attractants. The OSNs express IR92a, a member of the chemosensory ionotropic receptor (IR) family and project to a pair of glomeruli in the antennal lobe, termed VM1. In vivo calcium-imaging experiments showed that the OSNs and PNs innervating VM1 were activated by ammonia and amines but not by nonamine odorants. Flies in which the IR92a + neurons or IR92a gene was inactivated had impaired amine-evoked physiological and behavioral responses. Tracing neuronal pathways to higher brain centers showed that VM1-PN axonal projections within the lateral horn are topographically segregated from those of V-PN and DC4-PN, which mediate innate avoidance behavior to carbon dioxide and acidity, respectively, suggesting that these sensory stimuli of opposing valence are represented in spatially distinct neuroanatomic loci within the lateral horn. These experiments identified the neurons and their cognate receptor for amine detection, and mapped amine attractive olfactory inputs to higher brain centers. This labeled-line mode of amine coding appears to be hardwired to attraction behavior.

Published
2013

19. Oesophageal Atresia

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

20. Over-Breathing

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

21. Otitis Media, Acute

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

22. Opioid Dependence

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

23. Odynophagia

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

24. Orthodeoxia-Platypnea Syndrome

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

25. Outer Membrane Carnitine Palmitoyl Transferase

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

26. Ornithine Transcarbamylase

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

27. Orthostatic Hypotensive Disorder, Familial, Streeten Type

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

28. Ocular Coloboma-Imperforate Anus Syndrome

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

29. Ophthalmoplegia, Chronic Progressive External and Kearns Sayre Syndrome

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

30. OCTN2 Transporter Deficiency

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

31. Ogilvie's Syndrome

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

32. Outlet Obstruction

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

33. Osteoarthritis: Developmental Dysplasia of the Hip

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

34. Osteogenesis Imperfecta

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

35. OL-EDA-ID

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

36. Osteomalacia (Hypophosphathemic Rickets)

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

37. Oro-facio-digital Syndrome Type I

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

38. Osteopathia Condensans Disseminata

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

39. Occipital Horn Syndrome

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

40. Obstructive Uropathies

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

41. Ocular Melanosis

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

42. Osebold-Remondini Syndrome

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

43. Oculopharyngeal Muscular Dystrophy

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

44. Obsessive-compulsive Personality Disorder

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

45. Osteogenesis Imperfecta Ocular Form

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

46. Osteomalacia, Tumor-induced

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

47. Obstructive Sleep Apnea

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

48. Orbicular Eczema

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

49. Ophthalmoplegia and Rimmed Vacuoles

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

50. Obstructive Cholestasis

Author

Marc Slawik, Felix Beuschlein, Katrina Light, Roger Mulder, Gordon Dent, Mark G. Buckley, Stephen T. Holgate, Rosalia Misseri, Kirstan K. Meldrum, Massimiliano Mirabella, Gabriella Silvestri, Thomas Frieling, Alexander K. C. Leung, Andrew L. Wong, Marcus Schmitt, Jürgen Kohlhase, Sevan Hopyan, William Lane M. Robson, Maria Judit Molnar, Andrew J. Saxon, Simone Schimpf, Stefan R. Bornstein, Regina Ensenauer, Arno Fuchshuber, Carlo Nunes, Michael Escudier, Jo Spencer, Miranda Lomer, Stephen Challacombe, Jeremy Sanderson, Manish Suneja, Christie P. Thomas, Donatella Granchi, Nicola Baldini, George E. Ehrlich, Matthew B. Dobbs, Yasuaki Nakagawa, James Hyland, Roland Staud, Rajiv Kumar, Mary H. Hohenhaus, Nananda F. Col, Miep Helfrich, Anna Villa, Jan Hellemans, Geert Mortier, Minrong Ai, Matthew L. Warman, Markus Pfister, Hans-Peter Zenner, and Stefan K. Plontke

Published
2009

Catalog

Books, media, physical & digital resources
See catalog results