The Maori foot exhibits differences in plantar loading and midfoot morphology to the Caucasian foot.

The question being addressed in the current study was whether the diabetic Maori foot was more or less prone to ulceration than the diabetic New Zealand Caucasian (NZC) foot. Harris mat and pedobarographic analyses were employed to assess static and dynamic foot morphology and plantar loading in 40 Maori and NZC diabetic and non-diabetic participants. Significantly higher peak pressures were exhibited by the diabetic Maori participants compared to their NZC peers at the central forefoot. Significantly higher static and dynamic arch index values and significantly higher sub-arch angle values were exhibited by the non-diabetic Maori participants compared to their NZC peers. The latter findings suggest that healthy Maori may have a predisposition towards having a flatter foot than healthy NZC, which may have footwear design implications.

M-cadherin-mediated cell adhesion and complex formation with the catenins in myogenic mouse cells.

M-cadherin is a member of the multigene family of calcium-dependent intercellular adhesion molecules, the cadherins, which are involved in morphogenetic processes. Amino acid comparisons between M-cadherin and E-, N-, and P-cadherin suggested that M-cadherin diverged phylogenetically very early from these classical cadherins. It has been shown that M-cadherin is expressed in prenatal and adult skeletal muscle. In the cerebellum, M-cadherin is present in an adherens-type junction which differs in its molecular composition from the E-cadherin-mediated adherens-type junctions. These and other findings raised the question of whether M-cadherin and the classical cadherins share basic biochemical properties, notably the calcium-dependent resistance to proteolysis, mediation of calcium-dependent intercellular adhesion, and the capability to form M-cadherin complexes with the catenins. Here we show that M-cadherin is resistant to trypsin digestion in the presence of calcium ions but at lower trypsin concentrations than E-cadherin. When ectopically expressed in LMTK- cells, M-cadherin mediated calcium-dependent cell aggregation. Finally, M-cadherin was capable of forming two distinct cytoplasmic complexes in myogenic cells, either with alpha-catenin/beta-catenin or with alpha-catenin/plakoglobin, as E-and N-cadherin, for example, have previously been shown to form. The relative amount of these complexes changed during differentiation from C2C12 myoblasts to myotubes, although the molecular composition of each complex was unaffected during differentiation. These results demonstrate that M-cadherin shares important features with the classical cadherins despite its phylogenetic divergence.

Involvement of M-cadherin in terminal differentiation of skeletal muscle cells.

Cadherins are a gene family encoding calcium-dependent cell adhesion proteins which are thought to act in the establishment and maintenance of tissue organization. M-cadherin, one member of the family, has been found in myogenic cells of somitic origin during embryogenesis and in the adult. These findings have suggested that M-cadherin is involved in the regulation of morphogenesis of skeletal muscle cells. Therefore, we investigated the function of M-cadherin in the fusion of myoblasts into myotubes (terminal differentiation) in cell culture. Furthermore, we tested whether M-cadherin might influence (a) the expression of troponin T, a typical marker of biochemical differentiation of skeletal muscle cells, and (b) withdrawal of myoblasts from the cell cycle (called terminal commitment). The studies were performed by using antagonistic peptides which correspond to sequences of the putative M-cadherin binding domain. Analogous peptides of N-cadherin have previously been shown to interfere functionally with the N-cadherin-mediated cell adhesion. In the presence of antagonistic M-cadherin peptides, the fusion of myoblasts into myotubes was inhibited. Analysis of troponin T revealed that it was downregulated at the protein level although its mRNA was still detectable. In addition, withdrawal from the cell cycle typical for terminal commitment of muscle cells was not complete in fusion-blocked myogenic cells. Finally, expression of M-cadherin antisense RNA reducing the expression of the endogenous M-cadherin protein interfered with the fusion process of myoblasts. Our data imply that M-cadherin-mediated myoblast interaction plays an important role in terminal differentiation of skeletal muscle cells.

[Acute ischaemia after osteosynthesis of the proximal thigh (author's transl)]. / Das Syndrom der akuten Ischämie nach Osteosynthese des proximalen Oberschenkels.

In consequence of the increasing osteosynthetic treatment of bone fractures we draw the attention to iatrogenic blood vessel injuries. Primary location is the proximal thigh. Most important is the clinical diagnosis of an acute ischaemia of the operated limb. An arteriographic diagnosis is not necessary, but the operation site should be explored immediately. Prevention of intraoperative lesions of great vessels consists of exact anatomic reposition of the bone fragments, a subtile osteosynthesis whereas the osteosynthesis material should not extend the bone cortex. Exact haemostasis should be performed, avoiding extending ligations. Intraoperative as well as postoperative control of peripheral pulses should never be omitted.