346 research outputs found
Neuorientierungen im Strukturwandel von Familie - Wege zur Realisierung von Lebensperspektiven?
Sammelrezension zu: (1) Wissenschaftlicher Beirat fĂŒr Familienfragen: Familiale Erziehungskompetenzen. Beziehungsklima und Erziehungsleistungen in der Familie als Problem und
Aufgabe. Weinheim; MĂŒnchen: Juventa 2005, 164 S. ISBN 3-7799-0321-0. (2) Manfred Neuffer: Case Management. Soziale Arbeit mit Einzelnen und Familien. Weinheim; MĂŒnchen: Juventa 2005, 231 S. ISBN 3-7799-0733-X. (3) Angelika Tölke, Karsten Hank (Hrsg.): MĂ€nner - Das "vernachlĂ€ssigte" Geschlecht
in der Familienforschung. Wiesbaden: VS-Verlag 2005, 272 S. ISBN 3-531-14495-2
De Graviditate Tubaria in Specie et de Graviditate Extrauterina in Genere:dissertatio inauguralis anatomico-physiologica
http://tartu.ester.ee/record=b2500534~S1*es
taff - InterdisziplinÀre Professionalisierung von angehenden Lehrer_innen und Schulsozialarbeiter_innen in schwierigen Praxissituationen
Lehramtsstudierende und Studierende der Sozialen
Arbeit begegnen sich in der Berufspraxis im
gemeinsamen Arbeitsfeld Schule. In der Regel haben
sie vorher keine Erfahrungen mit der jeweils
anderen Profession gemacht und mĂŒssen in der
zunehmend multiprofessionellen Organisation
Schule diverse Herausforderungen meistern. Das
hier dargestellte Projekt âtaffâ möchte mit Hilfe des
didaktischen Ansatzes Problemorientiertes Lernen
dazu beitragen, dass sich die Studierenden möglichst
frĂŒh bereits im Studium mit der Lösung möglicher
Praxisprobleme interdisziplinÀr auseinandersetzen
können, um spÀter taff im Umgang mit
Kooperation und Problemlösung zu sein
Structural-Functional Interactions in the Therapeutic Response of Diabetic Neuropathy
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73587/1/j.1464-5491.1993.tb00195.x.pd
The Relative Contributions of the Medial Sural and Peroneal Communicating Nerves to the Sural Nerve
The medial sural cutaneous nerve (MSCN) and peroneal communicating nerve (PCN) conjoin in the calf area to form the sural nerve (SN). In previous anatomic studies, there was unresolved debate as to the main contributor to the sural nerve, and the relative contributions of MSCN and PCN had not been studied. The purpose of this study is to determine their relative neurophysiologic contributions to the SN by nerve conduction study (NCS). A total of 47 healthy subjects (25 males and 22 females, mean age 29.6 ± 10.4 yrs, range 20-59 yrs) participated in the study. This study employed the orthodromic nerve conduction technique: stimulation at the ankle and recording at the mid calf (SN); specifically, we preformed stimulation at the mid calf (MSCN, PCN) and recording at 14 cm proximal to the middle of the popliteal fossa (MSCN) and fibular head (PCN). The onset and peak latencies (ms) were SN 2.3 ± 0.2 and 3.0 ± 0.2; MSCN 2.1 ± 0.2 and 2.8 ± 0.2; and PCN 2.1 ± 0.2 and 2.8 ± 0.2. The peak-to-peak amplitudes (”V) and areas (nVsec) of the SN, MSCN, and PCN were 9.7 ± 3.9, 7.0 ± 4.7, and 5.0 ± 3.2; and 7.2 ± 2.9, 5.7 ± 3.4, and 4.0 ± 2.4, respectively. The side-to-side difference was not statistically significant. The main contributor to the SN was found to be the MSCN. The relative contribution ratio of the MSCN to the PCN was 1.37:1 by amplitude and 1.42:1 by area. However, in 32.9% of the subjects, the contribution of the PCN was greater than that of the MSCN
Diabetic polyneuropathies: update on research definition, diagnostic criteria and estimation of severity
Prior to a joint meeting of the Neurodiab Association and International Symposium on Diabetic Neuropathy held in Toronto, Ontario, Canada, 13â18 October 2009, Solomon Tesfaye, Sheffield, UK, convened a panel of neuromuscular experts to provide an update on polyneuropathies associated with diabetes (Toronto Consensus Panels on DPNs, 2009). Herein, we provide definitions of typical and atypical diabetic polyneuropathies (DPNs), diagnostic criteria, and approaches to diagnose sensorimotor polyneuropathy as well as to estimate severity. Diabetic sensorimotor polyneuropathy (DSPN), or typical DPN, usually develops on longâstanding hyperglycaemia, consequent metabolic derangements and microvessel alterations. It is frequently associated with microvessel retinal and kidney diseaseâbut other causes must be excluded. By contrast, atypical DPNs are intercurrent painful and autonomic smallâfibre polyneuropathies. Recognizing that there is a need to detect and estimate severity of DSPN validly and reproducibly, we define subclinical DSPN using nerve conduction criteria and define possible, probable, and confirmed clinical levels of DSPN. For conduct of epidemiologic surveys and randomized controlled trials, it is necessary to preâspecify which attributes of nerve conduction are to be used, the criterion for diagnosis, reference values, correction for applicable variables, and the specific criterion for DSPN. Herein, we provide the performance characteristics of several criteria for the diagnosis of sensorimotor polyneuropathy in healthy subjectâ and diabetic subject cohorts. Also outlined here are staged and continuous approaches to estimate severity of DSPN. Copyright © 2011 John Wiley & Sons, Ltd.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/87100/1/1226_ftp.pd
Charcot-Marie-Tooth Disease: Seventeen Causative Genes
Charcot-Marie-Tooth disease (CMT) is the most common form of inherited motor and sensory neuropathy. Moreover, CMT is a genetically heterogeneous disorder of the peripheral nervous system, with many genes identified as CMT-causative. CMT has two usual classifications: type 1, the demyelinating form (CMT1); and type 2, the axonal form (CMT2). In addition, patients are classified as CMTX if they have an X-linked inheritance pattern and CMT4 if the inheritance pattern is autosomal recessive. A large amount of new information on the genetic causes of CMT has become available, and mutations causing it have been associated with more than 17 different genes and 25 chromosomal loci. Advances in our understanding of the molecular basis of CMT have revealed an enormous diversity in genetic mechanisms, despite a clinical entity that is relatively uniform in presentation. In addition, recent encouraging studies - shown in CMT1A animal models - concerning the therapeutic effects of certain chemicals have been published; these suggest potential therapies for the most common form of CMT, CMT1A. This review focuses on the inherited motor and sensory neuropathy subgroup for which there has been an explosion of new molecular genetic information over the past decade
The reproducibility and sensitivity of sural nerve morphometry in the assessment of diabetic peripheral polyneuropathy
The nerve fibre loss, atrophy and injury of diabetic peripheral polyneuropathy and their responses to metabolic intervention have been studied by morphometric analysis of sural nerve biopsies. The magnitudes and sources of intra- and inter-individual variation in these morphometric measures have not been investigated previously in a systematic manner. Morphometric parameters of nerve fibre damage were measured in four separate fascicles from bilateral sural nerve specimens obtained post-mortem from 13 diabetic and 13 non-diabetic subjects. Intra- and inter-individual coefficients of variation were computed and compared to the magnitude of the differences between normal and diabetic subjects. Several morphometric variables emerged as highly sensitive and reproducible measures of nerve fibre damage suitable for clinical studies of diabetic peripheral polyneuropathy. These observations provide a rational basis for the design of future clinical trials employing morphometric end-points.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46025/1/125_2004_Article_BF00400485.pd
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