Neuorientierungen im Strukturwandel von Familie - Wege zur Realisierung von Lebensperspektiven?

Sammelrezension zu: (1) Wissenschaftlicher Beirat für Familienfragen: Familiale Erziehungskompetenzen. Beziehungsklima und Erziehungsleistungen in der Familie als Problem und Aufgabe. Weinheim; München: Juventa 2005, 164 S. ISBN 3-7799-0321-0. (2) Manfred Neuffer: Case Management. Soziale Arbeit mit Einzelnen und Familien. Weinheim; München: Juventa 2005, 231 S. ISBN 3-7799-0733-X. (3) Angelika Tölke, Karsten Hank (Hrsg.): Männer - Das "vernachlässigte" 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 - Interdisziplinäre 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 müssen in der zunehmend multiprofessionellen Organisation Schule diverse Herausforderungen meistern. Das hier dargestellte Projekt „taff“ möchte mit Hilfe des didaktischen Ansatzes Problemorientiertes Lernen dazu beitragen, dass sich die Studierenden möglichst früh bereits im Studium mit der Lösung möglicher Praxisprobleme interdisziplinär auseinandersetzen können, um später 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 (µV) 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, 13‐18 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 long‐standing hyperglycaemia, consequent metabolic derangements and microvessel alterations. It is frequently associated with microvessel retinal and kidney disease—but other causes must be excluded. By contrast, atypical DPNs are intercurrent painful and autonomic small‐fibre 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 pre‐specify 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 subject‐ 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

Doença de Charcot-Marie-Tooth: estudo da biópsia do nervo sural em 41 pacientes

São apresentados os resultados da biópsia do nervo sural à microscopia óptica e eletrônica (ME) em 41 pacientes com doença de Charcot-Marie-Tooth (CMT) Por estudos de neurocondução prévios nove eram do tipo I e 32 do tipo II. No tipo I, todos tinham grande diminuição do número de fibras, sendo os histogramas do tipo unimodal. Encontramos imagens de desmielinização, remielinização, formação de bulbos de cebola e de regeneração. Um paciente apresentava espessamento da bainha de mielina (atrofia axonal). No tipo II, sete pacientes não apresentavam anomalia à microscopia, com histograma normal. Nos restantes havia discreta a intensa perda de fibras mielínicas principalmente as de grande calibre. Em cinco enfermos havia aumento do número de fibras devido a grande regeneração. Alguns pacientes do tipo II apresentavam à ME imagens de pequenos bulbos de cebola e em um havia também atrofia axonal. Comparando com os dados clínicos e de neurocondução motora, no tipo I não encontramos relação entre a intensidade do quadro clínico e a perda de fibras mielínicas porém houve paralelismo da queda da neurocondução motora e a diminuição do número de fibras. No tipo II não houve relação entre o quadro clínico, a neurocondução e os achados da biópsia nervosa.We studied the pathological findings of sural nerve biopsy in 41 patients with Charcot-Marie-Tooth (CMT) disease. They were previously classified by the median motor conduction velocity (MCV) in two types. Type I (demyelinating) with 9 patients and type II (axonal) with 32 cases. In type I we found loss of myelinated fibers (unimodal histogram), demyelinated and remyelinated axons with numerous onion bulb formations. In one case there was thickness of myelin with thin axons (axonal atrophy). In type II there were seven patients with normal sural nerve biopsy. In 25 cases there were mild to severe loss of myelinated fibers. In 5 patients the number of myelinated fibers was increased due to the great regeneration of the axons. The electron microscopic studies in type II showed in a few cases small onion bulbs and in one case axonal atrophy. In type I there was no correlation between clinical severity and the loss of myelinated fibers, but there was relationship between the low MCV and the intensity of myelinated fibers. In type II we did not found any correlation between clinical course, MCV and pathological findings

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