Guinea pig models for translation of the developmental origins of health and disease hypothesis into the clinic

Over 30 years ago Professor David Barker first proposed the theory that events in early life could explain an individual\u27s risk of non-communicable disease in later life: the developmental origins of health and disease (DOHaD) hypothesis. During the 1990s the validity of the DOHaD hypothesis was extensively tested in a number of human populations and the mechanisms underpinning it characterised in a range of experimental animal models. Over the past decade, researchers have sought to use this mechanistic understanding of DOHaD to develop therapeutic interventions during pregnancy and early life to improve adult health. A variety of animal models have been used to develop and evaluate interventions, each with strengths and limitations. It is becoming apparent that effective translational research requires that the animal paradigm selected mirrors the tempo of human fetal growth and development as closely as possible so that the effect of a perinatal insult and/or therapeutic intervention can be fully assessed. The guinea pig is one such animal model that over the past two decades has demonstrated itself to be a very useful platform for these important reproductive studies. This review highlights similarities in the in utero development between humans and guinea pigs, the strengths and limitations of the guinea pig as an experimental model of DOHaD and the guinea pig\u27s potential to enhance clinical therapeutic innovation to improve human health. (Figure presented.)

Die klaffende Tube: Langzeitergebnisse nach konservativer Therapie

Einleitung: Für das Syndrom der klaffenden Tube steht bis heute keine standardisierte oder anhaltend erfolgreiche Therapie zur Verfügung. Auf der Basis des funktionellen Synergismus zwischen M. tensor veli palatini und M. pterygoideus medialis für die Tubenmechanik wurde ein neuer Therapieansatz entwickelt. Dieser besteht aus einer Dynamisierung und Stabilisierung insbesondere des M. pterygoideus medialis.Methodik: Anhand von 21 Patienten mit klaffender Tube werden Diagnostik, Therapie und Therapieerfolg nach einem Mindestzeitraum von 6 Monaten erläutert. Die Therapie des M. pterygoideus medialis basiert auf der Kombination einer Physiotherapie und der Anpassung einer zahnärztlichen Aufbissschiene, um den Muskel zu dynamisieren und zu kräftigen.Ergebnisse: Von den 21 Patienten wiesen nach sechswöchigem Training 7 keine Beschwerden mehr auf. 13 gaben posttherapeutisch ein so geringes Beschwerdemaß an, dass sie keine weitere Therapie für nötig erachteten. Bei einer Patientin konnte keine Verbesserung erreicht werden.Schlussfolgerung: Die muskuläre Therapie des M. pterygoideus medialis sollte aufgrund der hohen langfristigen Erfolgsrate und nicht vorhandener Invasivität grundsätzlich die Therapie der Wahl darstellen. Obstruierende operative Maßnahmen sollten erst bei rezidivierter oder persistierender Symptomatik nach konservativer Therapie zum Einsatz kommen

Cavia porcellus as a Model for Experimental Infection by Trypanosoma cruzi

The guinea pig (Cavia porcellus) is a natural reservoir for Trypanosoma cruzi but has seldom been used as an experimental infection model. We developed a guinea pig infection model for acute and chronic Chagas disease. Seventy-two guinea pigs were inoculated intradermally with 104 trypomastigotes of T. cruzi strain Y (experimental group); 18 guinea pigs were used as control group. Eight animals from the experimental group and two from the control group were sacrificed 5, 15, 20, 25, 40, 55, 115, 165, and 365 days after inoculation. During the acute phase (15 to 55 days), we observed parasitemia (with a peak on day 20) and positive IgM and IgG Western blots with anti-shed acute-phase antigen bands. The cardiac tissue showed vasculitis, necrosis (on days 40 to 55), moderate to severe inflammation, and abundant amastigote nests. Smaller numbers of amastigote nests were also present in kidney, brain, and other organs. In the early chronic phase (115 to 165 days), parasitemia disappeared and anti–T. cruzi IgG antibodies were still detectable. In cardiac tissue, the number of amastigote nests and the grade of inflammation decreased. In the chronic phase (365 days), the cardiac tissue showed vasculitis and fibrosis; detectable parasite DNA was associated with higher grades of inflammation. The experimental T. cruzi infection model in guinea pigs shows kinetics and pathologic changes similar to those of the human disease