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1. Vocational Training Programs and Youth Labor Market Outcomes: Evidence from Nepal

Author

Chakravarty, S., Lundberg, M., Nikolov, P., and Zenker, J.

Subjects
Economics - Econometrics, Economics - General Economics
Abstract

Lack of skills is arguably one of the most important determinants of high levels of unemployment and poverty. In response, policymakers often initiate vocational training programs in effort to enhance skill formation among the youth. Using a regression-discontinuity design, we examine a large youth training intervention in Nepal. We find, twelve months after the start of the training program, that the intervention generated an increase in non-farm employment of 10 percentage points (ITT estimates) and up to 31 percentage points for program compliers (LATE estimates). We also detect sizeable gains in monthly earnings. Women who start self-employment activities inside their homes largely drive these impacts. We argue that low baseline educational levels and non-farm employment levels and Nepal's social and cultural norms towards women drive our large program impacts. Our results suggest that the program enables otherwise underemployed women to earn an income while staying at home - close to household errands and in line with the socio-cultural norms that prevent them from taking up employment outside the house.

Published
2020
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2. Epsilon tubulin is an essential determinant of microtubule-based structures in male germ cells

Author

Stathatos, GG, Merriner, DJ, O'Connor, AE, Zenker, J, Dunleavy, JEM, O'Bryan, MK, Stathatos, GG, Merriner, DJ, O'Connor, AE, Zenker, J, Dunleavy, JEM, and O'Bryan, MK

Abstract

Alpha, beta, and gamma tubulins are essential building blocks for all eukaryotic cells. The functions of the non-canonical tubulins, delta, epsilon, and zeta, however, remain poorly understood and their requirement in mammalian development untested. Herein we have used a spermatogenesis model to define epsilon tubulin (TUBE1) function in mice. We show that TUBE1 is essential for the function of multiple complex microtubule arrays, including the meiotic spindle, axoneme and manchette and in its absence, there is a dramatic loss of germ cells and male sterility. Moreover, we provide evidence for the interplay between TUBE1 and katanin-mediated microtubule severing, and for the sub-specialization of individual katanin paralogs in the regulation of specific microtubule arrays.

Published
2024

8. Die Rolle des Myelin Proteins 2 (P2) nach traumatischer Nervenverletzung – Eine in vitro und in vivo Studie

Author

Klingler, F, Jungbluth, P, Ingenhoven, K, Zenker, J, Chrast, R, Windolf, J, Kieseier, B, and Stettner, M

Subjects
Myelinscheide, ddc: 610, Myelin, Replantataion, Peripheres Nervensystem, Nervenverletzung, Amputation, 610 Medical sciences, Medicine, Nervenregeneration, P2, Protein 2
Abstract

Fragestellung: Nach einer traumatischen Nervenverletzung wird zur Regeneration ein komplexer Prozess von Ab- und Wiederaufbau der Nervenfasern und ihrer Hüllstrukturen in Gang gesetzt. Der Wiederaufbau der Myelinscheide beeinflusst dabei das funktionelle Ergebnis dieses Regenerationsvorganges. [zum vollständigen Text gelangen Sie über die oben angegebene URL], Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2016)

Published
2016
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12. Neu-Iran

Author

Zenker, J. Th.

Published
1879

15. A role of peripheral myelin protein 2 in lipid homeostasis of myelinating Schwann cells

Author

Zenker, J., Stettner, M., Ruskamo, S., Domenech-Estevez, E., Baloui, H., Medard, J.J., Verheijen, M.H.G., Brouwers, J.F., Kursula, P., Kieseier, B.C., Chrast, R., Molecular and Cellular Neurobiology, and Neuroscience Campus Amsterdam - Brain Mechanisms in Health & Disease

Subjects
Mice, Knockout, Mice, Inbred C3H, Cell Membrane, Fatty Acids, Neural Conduction, Myelin Basic Protein, Myelin P2 Protein, Sciatic Nerve, Mice, Inbred C57BL, Phenotype, nervous system, Animals, Homeostasis, RNA, Messenger, Schwann Cells, Myelin Sheath
Abstract

Peripheral myelin protein 2 (Pmp2, P2 or Fabp8), a member of the fatty acid binding protein family, was originally described together with myelin basic protein (Mbp or P1) and myelin protein zero (Mpz or P0) as one of the most abundant myelin proteins in the peripheral nervous system (PNS). Although Pmp2 is predominantly expressed in myelinated Schwann cells, its role in glia is currently unknown. To study its function in PNS biology, we have generated a complete Pmp2 knockout mouse (Pmp2(-/-) ). Comprehensive characterization of Pmp2(-/-) mice revealed a temporary reduction in their motor nerve conduction velocity (MNCV). While this change was not accompanied by any defects in general myelin structure, we detected transitory alterations in the myelin lipid profile of Pmp2(-/-) mice. It was previously proposed that Pmp2 and Mbp have comparable functions in the PNS suggesting that the presence of Mbp can partially mask the Pmp2(-/-) phenotype. Indeed, we found that Mbp lacking Shi(-/-) mice, similar to Pmp2(-/-) animals, have preserved myelin structure and reduced MNCV, but this phenotype was not aggravated in Pmp2(-/-) /Shi(-/-) mutants indicating that Pmp2 and Mbp do not substitute each other's functions in the PNS. These data, together with our observation that Pmp2 binds and transports fatty acids to membranes, uncover a role for Pmp2 in lipid homeostasis of myelinating Schwann cells.

Published
2014
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17. Consequences of modified lipid and glucose metabolism on peripheral nervous system structure and function

Author

Zenker, J.

Abstract

284 million people worldwide suffered from type 2 diabetes mellitus (T2DM) in 2010, which will, in approximately half of them, lead to the development of diabetic peripheral neuropathy (DPN). Although DPN is the most common complication of diabetes mellitus and the leading cause of non-traumatic amputations its pathophysiology is still poorly understood. To get more insight into the molecular mechanism underlying DPN in T2DM, I used a rodent model of T2DM, the db/db mice.¦ln vivo electrophysiological recordings of diabetic animals indicated that in addition to reduced nerve conduction velocity db/db mice also present increased nerve excitability. Further ex vivo evaluation of the electrophysiological properties of db/db nerves clearly established a presence of the peripheral nerve hyperexcitability (PNH) phenotype in diabetic animals. Using pharmacological inhibitors we demonstrated that PNH is mostly mediated by the decreased activity of Kv1 channels. ln agreement with these data 1 observed that the diabetic condition led to a reduced presence of the Kv1.2 subunits in juxtaparanodal regions of db/db peripheral nerves whereas its mANA and protein expression levels were not affected. Lmportantly, I confirmed a loss of juxtaparanodal Kv1.2 subunits in nerve biopsies from type 2 diabetic patients. Together these observations indicate that the type 2 diabetic condition leads to potassium-channel mediated changes of nerve excitability thus identifying them as potential drug targets to treat sorne of the DPN related symptoms.¦Schwann cells ensheath and isolate peripheral axons by the production of myelin, which consists of lipids and proteins in a ratio of 2:1. Peripheral myelin protein 2 (= P2, Pmp2 or FABP8) was originally described as one of the most abundant myelin proteins in the peripheral nervous system. P2, which is a member of the fatty acid binding protein (FABP) family, is a 14.8 kDa cytosolic protein expressed on the cytoplasmic side of compact myelin membranes. As indicated by their name, the principal role of FABPs is thought to be the binding and transport of fatty acids.¦To study its role in myelinating glial cells I have recently generated a complete P2 knockout mouse model (P2-/-). I confirmed the loss of P2 in the sciatic nerve of P2-/- mice at the mRNA and protein level. Electrophysiological analysis of the adult (P56) mutant mice revealed a mild but significant reduction in the motor nerve conduction velocity. lnterestingly, this functional change was not accompanied by any detectable alterations in general myelin structure. However, I have observed significant alterations in the mRNA expression level of other FABPs, predominantly FABP9, in the PNS of P2-/- mice as compared to age-matched P2+/+ mice indicating a role of P2 in the glial myelin lipid metabolism.¦Le diabète de type 2 touche 284 million de personnes dans le monde en 2010 et son évolution conduit dans la moitié des cas à une neuropathie périphérique diabétique. Bien que la neuropathie périphérique soit la complication la plus courante du diabète pouvant conduire jusqu'à l'amputation, sa physiopathologie est aujourd'hui encore mal comprise. Dans le but d'améliorer les connaissances moléculaires expliquant les mécanismes de la neuropathie liée au diabète de type 2, j'ai utilisé un modèle murin du diabète de type 2, les souris db/db.¦ln vivo, les enregistrements éléctrophysiologiques des animaux diabétiques montrent qu'en plus d'une diminution de la vitesse de conduction nerveuse, les souris db/db présentent également une augmentation de l'excitabilité nerveuse. Des mesures menées Ex­ vivo ont montré l'existence d'un phénotype d'hyperexcitabilité sur les nerfs périphériques isolés d'animaux diabétiques. Grâce à l'utilisation d'inhibiteurs pharmacologiques, nous avons pu démontrer que l'hyperexcitabilité démontrée était due à une réduction d'activité des canaux Kv1. En accord avec ces données, j'ai observé qu'une situation de diabète conduisait à une diminution des canaux Kv1.2 aux régions juxta-paranodales des nerfs périphériques db/db, alors que l'expression du transcrit et de la protéine restait stable. J'ai également confirmé l'absence de canaux Kv1.2 aux juxta-paranoeuds de biopsies de nerfs de patients diabétiques. L'ensemble de ces observations montrent que les nerfs périphériques chez les patients atteints de diabète de type 2 est due à une diminution des canaux potassiques rapides juxtaparanodaux les identifiant ainsi comme des cibles thérapeutiques potentielles.¦Les cellules de Schwann enveloppent et isolent les axones périphériques d'une membrane spécialisée, la myéline, composée de deux fois plus de lipides que de protéines. La protéine P2 (Pmp2 "peripheral myelin protein 2" ou FABP8 "fatty acid binding protein") est l'une des protéines les plus abondantes au système nerveux périphérique. P2 appartient à la famille de protéines FABP liant et transportant les acides gras et est une protéine cytosolique de 14,8 kDa exprimée du côté cytoplasmique de la myéline compacte.¦Afin d'étudier le rôle de P2 dans les cellules de Schwann myélinisantes, j'ai généré une souris knockout (P2-/-). Après avoir validé l'absence de transcrit et de protéine P2 dans les nerfs sciatiques P2-/-, des mesures électrophysiologiques ont montré une réduction modérée mais significative de la vitesse de conduction du nerf moteur périphérique. Il est important de noter que ces changements fonctionnels n'ont pas pu être associés à quelconque changement dans la structure de la myéline. Cependant, j'ai observé dans les nerfs périphériques P2-/-, une altération significative du niveau d'expression d'ARNm d'autres FABPs et en particulier FABP9. Ce dernier résultat démontre l'importance du rôle de la protéine P2 dans le métabolisme lipidique de la myéline.

Published
2012

18. TUBB5 and its disease-associated mutations influence the terminal differentiation and dendritic spine densities of cerebral cortical neurons

Author

Ngo, L., Haas, M., Qu, Z., Li, S., Zenker, J., Teng, K., Gunnersen, J., Breuss, M., Habgood, M., Keays, D., Heng, Julian, Ngo, L., Haas, M., Qu, Z., Li, S., Zenker, J., Teng, K., Gunnersen, J., Breuss, M., Habgood, M., Keays, D., and Heng, Julian

Abstract

© The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. The microtubule cytoskeleton is critical for the generation and maturation of neurons in the developing mammalian nervous system. We have previously shown that mutations in the ß-tubulin gene TUBB5 cause microcephaly with structural brain abnormalities in humans. While it is known that TUBB5 is necessary for the proper generation and migration of neurons, little is understood of the role it plays in neuronal differentiation and connectivity. Here, we report that perturbations to TUBB5 disrupt the morphology of cortical neurons, their neuronal complexity, axonal outgrowth, as well as the density and shape of dendritic spines in the postnatal murine cortex. The features we describe are consistent with defects in synaptic signaling. Cellular-based assays have revealed that TUBB5 substitutions have the capacity to alter the dynamic properties and polymerization rates of the microtubule cytoskeleton. Together, our studies show that TUBB5 is essential for neuronal differentiation and dendritic spine formation in vivo, providing insight into the underlying cellular pathology associated with TUBB5 disease states.

Published
2014

19. Asymmetrical Cranio-orbital Facial Stenosis

Author

B. Schaarschmidt, Hans Anderl, Mühlbauer W, Zenker J, Heeckt P, Höpner F, and Schmidt A

Subjects
Male, medicine.medical_specialty, Scoliosis, Craniosynostosis, Methods, Deformity, Humans, Medicine, Craniofacial skeleton, business.industry, Craniofacial Dysostosis, Infant, Newborn, Infant, medicine.disease, Surgery, Radiography, Stenosis, medicine.anatomical_structure, Female, medicine.symptom, Plagiocephaly, business, Wide resection, Follow-Up Studies, Orbit (anatomy)
Abstract

Cranio-orbital facial scoliosis is the result of unilateral premature stenosis of the craniofacial skeleton. Plagiocephaly is only a subform of the syndrome. The deformity progresses unless operative treatment is given. Operative treatment is indicated for functional, aesthetic, and psychosocial reasons. We advocate early operation in infancy (3 to 6 months) consisting of wide resection of the stenosed sutures of the cranium and orbit, repositioning, and remodeling relying on the spontaneous autodynamic reshaping of the nasoethmoidal complex and the midface structures during the course of further growth. In adolescents and adults, multisegmental osteotomies and remodeling into a definitive position are necessary.

Published
1991
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21. Anästhesie bei Patienten mit Anorexia nervosa und Bulimia nervosa.

Author

Zenker J, Hagenah U, Rossaint R, Zenker, J, Hagenah, U, and Rossaint, R

Abstract

Eating disorders are typical diseases of adolescence and early adulthood. About 1-3% of female juveniles suffer from anorexia nervosa (AN) or bulimia nervosa (BN). Today AN is still the psychiatric disease with the highest mortality rate. The peri-operative mortality rate of patients suffering from AN is in the range up to 15%. The beginning of AN is a lingering process and the majority of patients show increasingly restrictive eating habits ending in cachexia. Patients are obsessed by the predominant idea of being obese in spite of having a significant underweight. Patients suffering from bulimia break the strict regimen by eating enormous amounts of high calorie food. Such eating attacks are followed by weight reducing measures, mostly vomiting. Most of the physical changes caused by AN are due to starvation and loss of weight. The most significant medical complications are alterations of the cardiovascular system accompanied by decreasing contractility of the heart, bradycardia, electrocardiographic changes as well as disequilibrium of electrolytic and water balance. Most of these symptoms can be reversed by putting on weight. [ABSTRACT FROM AUTHOR]

Published
2010
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28. Measurements of tropospheric ozone with a compact UV DIAL system

Author

Chyba, Thomas H., primary, Zenker, J. Thomas, additional, McCray, Christophe L., additional, Lee, Hyung R., additional, Elivert, Roosevelt, additional, Thomas, Brandi, additional, Toppin, Crystal, additional, Larson, Dave, additional, Higdon, N. S., additional, Richter, Dale A., additional, and Fishman, Jack, additional

Published
1999
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39. SH3TC2, a protein mutant in Charcot-Marie-Tooth neuropathy, links peripheral nerve myelination to endosomal recycling.

Author

Stendel C, Roos A, Kleine H, Arnaud E, Ozçelik M, Sidiropoulos PN, Zenker J, Schüpfer F, Lehmann U, Sobota RM, Litchfield DW, Lüscher B, Chrast R, Suter U, Senderek J, Stendel, Claudia, Roos, Andreas, Kleine, Henning, Arnaud, Estelle, and Ozçelik, Murat

Abstract

Patients with Charcot-Marie-Tooth neuropathy and gene targeting in mice revealed an essential role for the SH3TC2 gene in peripheral nerve myelination. SH3TC2 expression is restricted to Schwann cells in the peripheral nervous system, and the gene product, SH3TC2, localizes to the perinuclear recycling compartment. Here, we show that SH3TC2 interacts with the small guanosine triphosphatase Rab11, which is known to regulate the recycling of internalized membranes and receptors back to the cell surface. Results of protein binding studies and transferrin receptor trafficking are in line with a role of SH3TC2 as a Rab11 effector molecule. Consistent with a function of Rab11 in Schwann cell myelination, SH3TC2 mutations that cause neuropathy disrupt the SH3TC2/Rab11 interaction, and forced expression of dominant negative Rab11 strongly impairs myelin formation in vitro. Our data indicate that the SH3TC2/Rab11 interaction is relevant for peripheral nerve pathophysiology and place endosomal recycling on the list of cellular mechanisms involved in Schwann cell myelination. [ABSTRACT FROM AUTHOR]

Published
2010
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41. Rhachistia; burnayi

Author

Zenker, J., Zenker, J., Zenker, J., and Zenker, J.

Abstract

http://name.umdl.umich.edu/IC-MOLLUSK1IC-X-127472%5DUMMZ-MOL-127453-127493, https://quod.lib.umich.edu/cgi/i/image/api/thumb/mollusk1ic/127472/UMMZ-MOL-127453-127493/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, contact the UMMZ Mollusks Division professional staff: mollusk1ic-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu.

42. Thapsia; troglodytes

Author

Zenker, J., Zenker, J., Zenker, J., and Zenker, J.

Abstract

http://name.umdl.umich.edu/IC-MOLLUSK1IC-X-127664%5DUMMZ-MOL-127658-127698, https://quod.lib.umich.edu/cgi/i/image/api/thumb/mollusk1ic/127664/UMMZ-MOL-127658-127698/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, contact the UMMZ Mollusks Division professional staff: mollusk1ic-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu.

43. Lanistes; lybicus

Author

Zenker, J., Zenker, J., Zenker, J., and Zenker, J.

Abstract

http://name.umdl.umich.edu/IC-MOLLUSK1IC-X-093255%5DUMMZ-MOL-93226-93266, https://quod.lib.umich.edu/cgi/i/image/api/thumb/mollusk1ic/093255/UMMZ-MOL-93226-93266/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, contact the UMMZ Mollusks Division professional staff: mollusk1ic-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu.

44. Potadoma; frethii

Author

Zenker, J., Zenker, J., Zenker, J., and Zenker, J.

Abstract

http://name.umdl.umich.edu/IC-MOLLUSK1IC-X-070342%5DUMMZ-MOL-70308-70344, https://quod.lib.umich.edu/cgi/i/image/api/thumb/mollusk1ic/070342/UMMZ-MOL-70308-70344/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, contact the UMMZ Mollusks Division professional staff: mollusk1ic-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu.

45. Pseudachatina; connectens

Author

Zenker, J., Zenker, J., Zenker, J., and Zenker, J.

Abstract

http://name.umdl.umich.edu/IC-MOLLUSK1IC-X-161050%5DUMMZ-MOL-161046-161086, https://quod.lib.umich.edu/cgi/i/image/api/thumb/mollusk1ic/161050/UMMZ-MOL-161046-161086/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, contact the UMMZ Mollusks Division professional staff: mollusk1ic-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu.

46. Limicolaria; numidica

Author

Zenker, J., Zenker, J., Zenker, J., and Zenker, J.

Abstract

http://name.umdl.umich.edu/IC-MOLLUSK1IC-X-140313%5DUMMZ-MOL-140285-140325, https://quod.lib.umich.edu/cgi/i/image/api/thumb/mollusk1ic/140313/UMMZ-MOL-140285-140325/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, contact the UMMZ Mollusks Division professional staff: mollusk1ic-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu.

47. Edentulina; liberiana

Author

Zenker, J., Zenker, J., Zenker, J., and Zenker, J.

Abstract

http://name.umdl.umich.edu/IC-MOLLUSK1IC-X-128343%5DUMMZ-MOL-128314-128353, https://quod.lib.umich.edu/cgi/i/image/api/thumb/mollusk1ic/128343/UMMZ-MOL-128314-128353/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, contact the UMMZ Mollusks Division professional staff: mollusk1ic-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu.

48. Pseudachatina; gravenreuthi

Author

Zenker, J., Zenker, J., Zenker, J., and Zenker, J.

Abstract

http://name.umdl.umich.edu/IC-MOLLUSK1IC-X-161047%5DUMMZ-MOL-161046-161086, https://quod.lib.umich.edu/cgi/i/image/api/thumb/mollusk1ic/161047/UMMZ-MOL-161046-161086/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, contact the UMMZ Mollusks Division professional staff: mollusk1ic-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu.

49. Trochozonites; ibuensis

Author

Zenker, J., Zenker, J., Zenker, J., and Zenker, J.

Abstract

http://name.umdl.umich.edu/IC-MOLLUSK1IC-X-161080%5DUMMZ-MOL-161046-161086, https://quod.lib.umich.edu/cgi/i/image/api/thumb/mollusk1ic/161080/UMMZ-MOL-161046-161086/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, contact the UMMZ Mollusks Division professional staff: mollusk1ic-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu.

50. Pseudachatina; martensi

Author

Zenker, J., Zenker, J., Zenker, J., and Zenker, J.

Abstract

http://name.umdl.umich.edu/IC-MOLLUSK1IC-X-161051%5DUMMZ-MOL-161046-161086, https://quod.lib.umich.edu/cgi/i/image/api/thumb/mollusk1ic/161051/UMMZ-MOL-161046-161086/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, contact the UMMZ Mollusks Division professional staff: mollusk1ic-dlps-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library Information Technology: libraryit-info@umich.edu.

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