Real-time three-dimensional jaw tracking in temporomandibular disorders.

When a dysfunction occurs in any component of the stomatognathic system, temporomandibular disorders (TMD) may originate. The aim of this study was to compare the deviations, displacement and the execution speed of mandibular movements among asymptomatic participants and those with TMD. Convenience sampling was used; forty participants diagnosed by clinical evaluation following the Research Diagnostic Criteria for Temporomandibular Disorders were divided into three groups: arthropathy (GART, 10 participants, 40% men), myopathy (GMYO, 10 participants, 30% men), and the control group (CG, 20 asymptomatic participants, 25% men). Participants were asked to perform the movements of free maximal mouth opening and closing, right and left lateral excursions, and protrusion with sliding teeth contacts. The mandibular trajectory was recorded using opto-electronic devices tracking reflective markers placed in front of the 'soft tissue pogonion point'. The movements were analysed on the following axis: x - medial-lateral, y - vertical, z - antero-posterior. Significative differences were found in CGxGART - unassisted maximal mouth opening and closing projection on y-axis (OCY), CGxGMYO - unassisted maximal mouth opening and closing projection on x-axis (OCX), and in the measures Opening lateral deviation on x-axis (OLDX), closing lateral deviation on x-axis (CLDX) and in the measures of speed for both. In regard to GARTxGMYO, a significative difference was found in Protrusion lateral deviation on x-axis (PLDX) 'Conover-Iman Test of Multiple Comparisons Using Rank Sums' using Bonferroni correction (P < 0·05). In conclusion, the total opening movements in individuals with TMD tended to have higher deviation than in those asymptomatic individuals and a reduction in the speed of movements.

Measurement of jaw motion: the proposal of a simple and accurate method.

The analysis of jaw movements has long been used as a measure for clinical diagnosis and assessment. A number of strategies are available for monitoring the trajectory; however most of these strategies make use of expensive tools, which are often not available to many clinics in the world. In this context, this research proposes the development of a new tool capable of quantifying the movements of opening/closing, protrusion and laterotrusion of the mandible. These movements are important for the clinical evaluation of both the temporomandibular function and muscles involved in mastication. The proposed system, unlike current commercial systems, employs a low-cost video camera and a computer program, which is used for reconstructing the trajectory of a reflective marker that is fixed on the jaw. In order to illustrate the application of the devised tool a clinical trial was carried out, investigating jaw movements of 10 subjects. The results obtained in this study were compatible with those found in the literature with the advantage of using a low-cost, simple, non-invasive and flexible solution customized for the practical needs of clinics. The average error of the system was less than 1.0%.

Stability from structure: metabolic networks are unlike other biological networks.

In recent work, attempts have been made to link the structure of biochemical networks to their complex dynamics. It was shown that structurally stable network motifs are enriched in such networks. In this work, we investigate to what extent these findings apply to metabolic networks. To this end, we extend a previously proposed method by changing the null model for determining motif enrichment, by using interaction types directly obtained from structural interaction matrices, by generating a distribution of partial derivatives of reaction rates and by simulating enzymatic regulation on metabolic networks. Our findings suggest that the conclusions drawn in previous work cannot be extended to metabolic networks, that is, structurally stable network motifs are not enriched in metabolic networks.

Mice lacking the vascular endothelial growth factor-B gene (Vegfb) have smaller hearts, dysfunctional coronary vasculature, and impaired recovery from cardiac ischemia.

Vascular endothelial growth factor-B (VEGF-B) is closely related to VEGF-A, an effector of blood vessel growth during development and disease and a strong candidate for angiogenic therapies. To further study the in vivo function of VEGF-B, we have generated Vegfb knockout mice (Vegfb(-/-)). Unlike Vegfa knockout mice, which die during embryogenesis, Vegfb(-/-) mice are healthy and fertile. Despite appearing overtly normal, Vegfb(-/-) hearts are reduced in size and display vascular dysfunction after coronary occlusion and impaired recovery from experimentally induced myocardial ischemia. These findings reveal a role for VEGF-B in the development or function of coronary vasculature and suggest potential clinical use in therapeutic angiogenesis.

Cell proliferation in mammalian gastrulation: the ventral node and notochord are relatively quiescent.

During gastrulation, the node of the mammalian embryo appears to be an organising centre, homologous to Hensen's node in the chick and the dorsal lip of the amphibian blastopore. In addition, the node serves as a precursor population for the head process, notochord and foregut endoderm. We have studied node architecture and cell morphology by electron microscopy, and cell proliferation using bromodeoxyuridine incorporation and mitotic counts. The dorsal (ectodermal) and ventral (endodermal) components of the node are two distinct populations, separated by a basement membrane. The ventral node, contiguous with the head process, is characterised by a relatively low proliferation rate, with only approximately 10% of cells incorporating BrdU over 4 hr, compared to > 95% in surrounding mesodermal and ectodermal tissues. This is the case from the beginning of node formation, at the no-allantoic-bud stage, until the 7 somite stage, and is not compatible with the idea that the ventral node is a stem cell population. The dorsal node is highly proliferative, its rate of division being indistinguishable from the neurectoderm, with which it is contiguous. In the ventral node, two regions can be recognised: cells in the "pit" are columnar and all monociliated; around them lies a "crown" of cells arranged radially in a horseshoe shape and less often ciliated. Node derivatives share common features with the ventral node; the head process and the notochord are relatively quiescent; and some head process cells are also monociliated. Node and head process monocilia are immotile and appear to be associated with non-proliferation. We suggest that the ventral node contains all the properties of the organiser, while the dorsal node is indistinct from the surrounding epiblast. The cranial end of the foregut pouch, the thyroid diverticulum, and the promyocardium of early somite stage embryos are also areas of low cell division. All the described regions of relative quiescence are sites of expression of members of the TGF beta family, which may be involved in maintaining non-proliferation.

Effects of ethanol and acetaldehyde on rat embryos developing in vitro.

Rat embryos were explanted on Days 9.5 or 10 of gestation and cultured for 48 to 30h, respectively, in rat serum containing 0, 3, 6, 9 mg/ml of Ethanol (Eth); 0, 10, 20 micrograms/ml of Acetaldehyde (Ach); 3 mg/ml Eth + 10 micrograms/ml Ach. At the end of the culture period the embryos were evaluated for vitality, and scored. Some of them were also examined histologically. Embryos exposed to Eth from Day 9.5 showed a dose-related growth retardation associated with a high frequency of malformations (open neural tube, heart defects, branchial arch hypoplasia). The exposure of 9.5-day embryos to 20 micrograms/ml Ach resulted in 100% embryolethality, whereas 10 micrograms/ml induced growth retardation and teratogenic effects. When 10-day embryos were exposed to 3 mg/ml Eth or 10 microliters/ml Ach no effects were observed, but the highest levels of Eth produced a moderate growth retardation and morphologic defects. Exposure to 20 micrograms/ml Ach induced hypoplasia of the first arch, but did not alter the score value. The histologic examination of these embryos revealed severe lesions at the level of the neuroepithelium and of the branchial mesenchyma. Similar effects were observed in embryos exposed simultaneously to 3 mg/ml Eth and 10 micrograms/ml Ach. These results should make us reevaluate the role of Ach in the Eth-induced embryopathies.