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T Pexieder

Publications and source records attributed to T Pexieder.

At least 37 records · Page 2Linked to original sources
PubMed1991

Pathogenesis of various forms of double outlet right ventricle in mouse fetal trisomy 13.

The pathogenesis of double outlet right ventricle with or without pulmonary infundibular atresia in mouse fetal trisomy 13 was studied at the organ level using microdissection and scanning electron microscopy. Altogether, 394 karyotyped trisomic embryos were collected between 11 days and 16 hours of gestation (presence of a vaginal plug = day 1) and 15 days of gestation at intervals of 8 hours, and at 16 days of gestation. The hearts were perfusion-fixed, microdissected, and prepared to be observed in scanning electron microscope in the following standardized orientations: frontal, right or left profile, septal and parietal halves of the right ventricle and outflow tract (conotruncus). Comparison of 276 trisomic hearts with their normal counterparts described previously has shown that: the first pathognomonic feature is the abnormal anterior position of the proximal part of the parietal outflow tract ridge or of both ridges (at 12 days and 16 hours of gestation); the abnormal anterior fusion of these ridges ("coalescence") results in a mesenchymal mass behind which is deviated the pulmonary part of the outflow tract lumen; from 14 days and 16 hours of gestation on, this lumen is either obstructed, resulting in a supravalvar stenosis of the pulmonary trunk and subsequently evolving into double outlet right ventricle with pulmonary infundibular atresia; or, in a minority of cases, this lumen is not obstructed and the heart develops into double outlet right ventricle without pulmonary infundibular atresia. The pathogenesis of these malformations differs from most of the known hypotheses based on deductions from human malformed hearts, as well as from observations of the pathogenesis of similar outflow tract malformations, such as those found in the Keeshond dog or rats treated with trimethadione.

Animals↗
PubMed1990

Variations in microscopic anatomy and ultrastructure of human embryonic hearts subjected to three different modes of fixation.

The external form and the internal contour of the ventricular surfaces were studied in human embryonic hearts following three modes of fixation: A) simple immersion fixation, B) indirect ventricular perfusion through the umbilical vein and C) high flow-low pressure ventricular perfusion-inflation. Fixation artifacts, resulting in distortion of the external form of the heart together with distortion of the internal contour of the ventricular cavities, were observed in specimens submitted to modes A and B of fixation. By contrast, hearts fixed by direct ventricular perfusion-inflation (C), showed less distortion in their external form, and the various intraventricular components maintained their spatial relationship among themselves and with the great arteries. Thus, reproducible developmental anatomical features at organ and tissue levels were readily available for study. The relevance of a direct ventricular perfusion-fixation method is discussed in relation to the value of human cardiac developmental data obtained in the past, after using simple immersion, or other modes of fixation.

Heart↗
PubMed1990

[Pathogenesis of congenital heart defects: fiction and truth].

This is a review based on a description of a standardized method (microdissection + SEM) for study of human and animal cardiac development. Two examples of the analytical approach are given. In the first one, concerning the establishment of contact between the aorta and the left ventricle, the previous assumptions for "vectorial bulbus rotation" are disproved by more precise observations of normal cardiac development. Aorta is not transferred into the left ventricle but is connected to it by means of a "conduit" (aortic vestibulum) delimited by the fusion of the conotruncus ridges. For the second example the multilevel-analysis of pathogenesis of conotruncus septum defects in Keeshond dogs was selected. At the organ level, hypoplasia of the right ventricle was diagnosed, accompanied by hypoplasia of conus cushions. Tissue-level analysis indicated that the major cause of these hypoplasias is a decreased relative volume of the myocardium. Further study at the cell level showed that the number of mesenchymal cells in certain parts of conotruncus cushions is also diminished. Combining these observations with what is known about the architecture of cell proliferation in the embryonic heart, allows to formulate a hypothesis on a selective lesion of the right proliferation center, as one of the main causes of the observed anomalies. Further progress towards the subcellular and molecular level will help to complete the pathway from a gene defect toward an organ defect.

Animals↗
PubMed1989

Normal stages of cardiac organogenesis in the mouse: I. Development of the external shape of the heart.

Normal development of the mouse embryonic heart was studied at the organ level using microdissection and scanning electron microscopy (SEM). Altogether 225 embryos, sampled at 8-hour intervals between 11ed (ed = embryonic day; day of vaginal plug = 1ed) and 15ed were collected. Their hearts were fixed by high flow-low pressure perfusion, microdissected, and observed in SEM. Standardized frontal, right profile, and left profile SEM micrographs were obtained and analyzed. The main purpose of this study was to create a series of normal stages of mouse cardiac development as a reference for ongoing studies in experimental cardiac teratology (e.g., in fetal mouse trisomies). Comparisons with chick, human, and dog embryonic hearts, prepared using the same technique, show that the mouse embryonic heart is characterized by a relatively deep interventricular sulcus. The absence of a conoventricular sulcus in the mouse results in poor definition of the boundary between the conus and the right ventricle. The external separation of the aorta and the pulmonary artery is evident from 13ed onward. The respective positions of the great arteries (aorta dextroposterior, pulmonary artery sinistroanterior) does not change until the end of cardiac organogenesis (15ed in the mouse).

Animals↗
PubMed1989

Normal stages of cardiac organogenesis in the mouse: II. Development of the internal relief of the heart.

Normal stages of intracardiac development of the mouse heart are illustrated by a collection and analysis of two complementary SEM views, the septal and parietal halves of the right ventricle and conotruncus. These views are particularly suitable for understanding the septation of the outflow tract of the heart. They represent references for the studies of the pathogenesis of conotruncal malformations. The analysis is based on 90 hearts between 11ed and 15ed at intervals of 8 hours with an additional stage at 16ed. They were prepared by perfusion fixation, microdissection, and critical point drying and were examined in SEM. The following main features of the intracardiac morphogenesis were observed: 1) the presence of two spirally positioned conotruncal ridges, their disto-proximal fusion, and the formation of the semilunar valves at their distal part; 2) the trabecular transformation of the conotruncal wall; and 3) the presence of two different interventricular foramina (FIV II and FIV III), with the final closure of FIV III at 14ed16h-15ed. As a result of these observations, our description of the outflow tract septation and its interpretation are different from other conceptions based on mechanisms such as bulbar shift, bulbar absorption, torsions, or transfer of the aorta into the left ventricle.

Animals↗
PubMed1986

Rabbit oviduct mucosa healing after accidental transmucosal suture passage.

The purpose of this study is to show by SEM the characteristics of mucosal healing related to the presence of intraluminal sutures of nylon (nonabsorbable) or dexon (absorbable) in the rabbit oviduct. Altogether, 30 animals with anastomosis in the isthmus were killed 2, 4, 8, or 12 weeks after the operation. Tubular structures or pieces of thread partially or completely covered by the epithelium were found n 36.8% of these cases. Independently of the suture material used, already 2 weeks after surgery, the thread was covered by an epithelium composed mostly of squamous cells and some rare ciliated cells. At 4 weeks, the proportion of ciliated cells was increased. Regions with the usual cellular morphology and repartition of the different cellular types were also observed. However, at 8 and 12 weeks, islets of atypical squamous cells persisted in areas of transmucosal passage of the suture material. At 12 weeks, the dexon suture was not yet completely absorbed.

Animals↗
PubMed1986

Stereomicroangiography in embryologic and teratologic investigation.

Vascular dysmorphogenesis is usually investigated by invasive microdissection or time-consuming reconstruction of serial sections. Stereomicroangiography (SMA) was used for detection and analysis of vascular abnormalities in a murine trisomy 13 model demonstrating pulmonary atresia. Twenty-two litters from doubly heterozygous Robertsonian translocation Rb(6.13)3Rma/Rb(5.13)70Lub male matings to NMRI females were studied. Embryos (13-17 days gestation) were prepared by umbilical vein perfusion with buffered fixative and umbilical artery perfusion with 5% AgNO3. After immersion fixation specimens were infiltrated with paraffin, mounted on stubs, and stereoradiographed at multiple angles. Transverse serial sections were prepared of the thoracic area. Thoracic vascular morphology was satisfactorily imaged and trisomy 13 embryos were correctly distinguished from normals in 105 of 120 embryos (87.5%). When independent SMA and histologic interpretations were compared anomalous vasculature was correctly identified in all 27 trisomic embryos and one control, and falsely interpreted in one normal embryo. Normal vascular morphology was demonstrated in the remaining 76 normal embryos. Separate SEM evaluation of five microdissected hearts from nontrisomic embryos following this perfusion schedule showed normal distension of the ventricular cavity and metallic silver deposition on the surface and at junctions of endocardial cells. Light microscopy revealed silver staining at the endothelial surface and within the endocardial cushions. SMA accurately records embryonic vascular morphology for rapid screening of viable embryos.

Angiography↗
PubMed1985

Antisperm antibodies and in vitro fertilization failure.

A new enzyme-linked immunosorbent assay (ELISA)-based test (Zer, Jerusalem) has allowed us to show the presence of antisperm antibodies (1:32 to 1:64) in the blood of 14 (33%) of 32 patients undergoing in vitro fertilization and embryo transfer (IVF-ET) under gonadotropin stimulation. Observation of the morphology of fertilization in eight patients with and seven patients without antisperm antibodies has shown a significant association (P less than or equal to 0.025, Fisher exact probability test) among the cumulus/corona coagulation, the absence of fertilization, and the presence of these antibodies. Cumulus/oocyte complex washing and/or enzymatic cumulus removal are considered as elective interventions in the case of antisperm immunity. Each patient entering an IVF-ET program should have the antisperm antibody assay performed as a preliminary screening.

Antibodies↗
PubMed1981

Prenatal development of the endocardium: a review.

The chronology of SEM studies of the embryonic endocardium is followed in this review by discussion of species, stages and localizations studied. In reviewing the methodology of SEM studies of the embryonic endocardium, particular weight is given to standard methods which can be applied to all species of interest. Two main aspects are more deeply analysed: the perfusion fixation and the effects of the osmolarity of the fixative vehicle. Using these standardized techniques, the embryonic endocardium of chick, mouse, dog, human and, to a lesser extent, rat hearts are described in SEM. All species investigated presented microvilli ruffles, filopodia, cytosegresomes, intercellular openings and phagocytes. Marginal folds, lamellipodia, dividing cells and incomplete endocardium could be observed in some species only. Each of these microappendages is discussed in relationship to observations of other authors on four levels - embryonic endocardium, adult endocardium, embryonic endothelium and adult endothelium. The general tendency in differentiation of the embryonic endocardium results in a progressive loss of the majority of the microappendages mentioned. Contrary to a relative absence of interspecific differences in endocardial morphology as seen in SEM, there is a strong variation of this morphology relating to the intracardiac localization of the endocardial cells. The discovery of autolytic postmortem changes in the material from pregnancies terminated by prostaglandins leads to the recommendation that the further use of this source of embryonic and fetal material be discouraged. Finally, the modifications of the morphology of embryonic endocardial cells under the effects of cytochalasin B, altered hemodynamics, and the hereditary congenital heart defects of the Keeshond strain of dogs are discussed, using the above-mentioned principles of four levels.

Animals↗
PubMed1979

Changing scene in cardiac embryology.

Recent significant advances in experimental embryology and experimental teratology of the heart contribute to the renaissance in studies of cardiac development. Examples taken from the author's laboratory demonstrate the need for reference points in the description of heart morphogenesis and speak against the existence of conus resorption. The discovery of animal models of congenital heart disease, e.g. Keeshond dog or fetal mouse trisomy, represent another promising opening in studies of pathogenesis of heart anomalies. To permit a reasonable understanding of the univentricular heart following basic questions need to be answered: a) what is the origin of its rudimentary cavity, b) what is the origin of its incomplete muscular septum, c) why are one or both great vessels attached to the rudimentary chamber, d) what determines the position of the rudimentary chamber and e) why may the great vessels be normally or abnormally arranged? The experimental analysis of the proliferative and growth pattern of the right ventricle as well as the studies on embryonic hemodynamic factors are presented as examples of how to approach these fundamental questions.

Age Factors↗