Search PubMed⌕ Search

Biomedical subjects

M Peterka

Publications and source records attributed to M Peterka.

At least 19 recordsLinked to original sources
PubMed2001

Systematics and evolution of ruminal species of the genus Prevotella.

Bacterial species of the genus Prevotella represent a numerically dominant microbial population in the rumen of cattle. They belong to the phylogenetic division Cytophaga-Flexibacter-Bacteroides (CFB) which is a large group of ecologically diverse bacteria with only a few shared traits. The phylogenetic descent from a common ancestor seems to be unquestionable, however, as judged from the small subunit ribosomal RNA analysis. Only 4 ruminal Prevotella species have been described to date, even though the sequence analysis of directly retrieved 16S rRNA genes indicates a large genetic diversity within this group of rumen bacteria. The closest relatives of ruminal Prevotella spp. are not surprisingly other species of the genus Prevotella, typically inhabiting the gastrointestinal tract, oral cavity and genital areas of other animals and man. The previous phylogenetic analysis showed that species of the genus Prevotella can be split into two groups or superclusters, the "ruminal" and the "non-ruminal prevotellas". One of 4 currently described ruminal Prevotella spp., i.e. P. albensis, has been placed outside the supercluster containing ruminal Prevotella spp. and within the supercluster containing the non-ruminal Prevotella spp. However, the number of available small subunit rRNA sequences from this species represents only a fraction of all known ruminal Prevotella sequences.

Animals↗
PubMed2001

Ribosomal RNA genes from Prevotella bryantii: organization and heterogeneity.

Five P. bryantii B(1)4 16S rRNA gene copies and their flanking regions were cloned and analyzed. A genomic library was constructed and screened with oligonucleotide DNA probe specific for 16S rRNA gene of P. bryantii. Five out of six different copies of 16S RNA gene were recovered and sequenced. Only minor differences (0.3-1.2%) between copies were detected within the 1541 bp long sequence. The impact of the sequence variability of 16S rRNA gene copies on phylogenetic positioning of P. bryantii was determined. All five sequences from cloned P. bryantii B(1)4 16S rRNA genes were placed in the same operational taxonomy unit. Control regions of all five analyzed rRNA operons were almost identical and three candidate for promoter sequences were identified by Neutral Network Promoter Prediction. Spacer regions between 16S rRNA and 23S rRNA genes in all five cloned copies were 543 bp long and genes for tRNA(Ile) and tRNA(Ala) were identified inside this regions.

Base Sequence↗
PubMed2001

Embryotoxicity of TPPS4 and PS 3 photosensitizers in chicken embryo under different light conditions.

Hematoporphyrin derivatives have been recommended for photodynamic therapy of malignant processes. We administered TPPS4, and Photosan 3 (PS 3) in chick embryo in ovo, with or without subsequent blue light (400-550 nm) irradiation. The aim was to analyze and compare the effects of both substances on organogenesis under different light conditions. The embryotoxic effect (embryonic death and malformations) was detected after a single intra-amniotic injection of 5 different doses (0.3 to 300 microg) of TPPS4 or PS 3 at embryonic day 3-5. The beginning of the embryotoxicity range (minimal embryotoxic dose) was determined in non-irradiated embryos to be between 0.3-3.0 microg PS 3 and 3.0-30.0 microg TPPS4. Malformations of surviving embryos were similar after both substances, represented by trunk hyperlordosis combined with incomplete closure of the ventral body wall and protrusion of viscera as consequences of amnion contraction, reduction limb deformities, eye malformations and cleft beak. Ten minutes light irradiation in ovo following two hours after intra-amniotic injection of TPPS4 or PS 3 increased by one order of magnitude their embryotoxic effects. Even dark-ineffective doses became highly embryotoxic. Contraction of the amniotic sac and extraembryonic vessels seemed to be a common mechanism of photosensitizer action.

Abnormalities, Drug-Induced↗
PubMed2000

The presence of rudimentary odontogenic structures in the mouse embryonic mandible requires reinterpretation of developmental control of first lower molar histomorphogenesis.

In the mouse embryonic maxilla, rudimentary tooth primordia have been identified, which can be mistaken for the first upper molar. In order to determine whether such a situation might exist in the lower jaw as well, tooth development was investigated in the mouse mandibular cheek region during ED 12.5-15.0. A combination of histology, morphometry and computer-aided 3D reconstructions demonstrated the existence of rudimentary dental structures, whose gradual appearance and regression was associated with the segmental progress of odontogenesis along the mesio-distal axis of the jaw: 1) At ED 12.5, the mesial segment (MS) was the most prominent part of the dental epithelial invagination. It included an asymmetrically budding dental lamina. The MS, although generally mistaken for the lower first molar (M1, primordium, regressed and did not finally participate in M1 cap formation. 2) At ED 13.5, a wide dental bud (called segment R2) appeared distally to the MS. Although the R2 segment transiently represented the predominant part of the dental epithelium at ED13.5, it participated only in the formation of the mesial end of the M1 cap. 3) The top of the R2 segment at ED13.5 was not the precursor of the enamel knot (EK), contrary to what has been assumed. 4) The central segment of the M1 cap as well as the EK developed later and distally to the R2 segment. 5) Time-space specific apoptosis correlated with the retardation in growth of the R2 segment as well as with strong regressive changes in the epithelium situated mesially to it. These highlight the need to reinterpret current molecular data on early M1 development in the mouse in order to correlate the expression of signalling molecules with specific morphogenetic events in the appropriate antemolar or molar segments of the embryonic mandible.

Animals↗
PubMed2000

Significant differences in the incidence of orofacial clefts in fifty-two Czech districts between 1983 and 1997.

Between 1983 and 1997 a total of 2029 children with CL/P (cleft lip, cleft lip and palate or cleft palate), who were born in the Bohemian districts of the Czech Republic and who underwent surgery and treatment at the Clinic of Plastic Surgery in Prague, were analysed. One possibility for decreasing the risk of delivery of a child with CL/P is to decrease or eliminate its prenatal exposure to embryotoxic factors. Detection of the embryotoxic factors acting at the individual level (e.g. elevated temperature, drug consumption, x-ray examination or infection) is easier than the detection of embryotoxic factors operating at the population level (e.g. water contamination, air pollution). When searching for the latter factors, we first have to reveal regional differences in CL/P incidence. The aim of the present paper was to determine significant differences in the mean incidence of newborns with CL/P in Bohemian districts during a 15 year period. The correlation between the incidence of CL/P and the birth rate in the different districts was also examined. The mean incidence of CL/P in all Bohemian districts was 1.86 per 1000 newborns (1.86/1000). Districts were divided into three groups, according to significant differences in the incidence of CL/P using a confidence interval. The lowest mean incidence of CL/P was detected in the Svitavy district (0.72/1000) and Louny (1.05/1000). The highest mean incidence was found in the Beroun district (2.86/1000). Besides Beroun, a high mean incidence of CL/P (more than 1.96/1000) was also found in Klatovy, Mĕlník, Tábor, Kolín, Semily, Ceská Lípa, Pardubice, Teplice, Ceský Krumlov, Sokolov, Chomutov, Praha-západ, Jicín, Rakovník, Kladno, Prachatice, Rokycany, Tachov, Liberec, Pelhrimov. Paradoxically, the districts with a higher or lower birth rate exhibited a lower (1.62/1000) or higher (1.92/1000) incidence of CL/P, respectively. Future studies should elucidate whether the significant regional differences in the incidence of CL/P can be related to differing exposure of pregnant women to harmful environmental embryotoxic factors.

Birth Rate↗
PubMed1999

Initial features of the inner dental epithelium histo-morphogenesis in the first lower molar in mouse.

First lower molar development in the mouse was investigated from the cap to early bell stage using histology, morphometry, TEM and 3D reconstructions. This period was characterized by the histogenesis of the enamel organ (EO), folding of the epithelio-mesenchymal junction and growth of the tooth. The histogenesis of the EO and appearance of the enamel knot (EK) were initiated at the early cap stage (ED14). From ED14 to ED15, the anterior and posterior extension of the EK was very prominent whilst the length of the enamel organ did not substantially change. The EK appeared as a dynamic and transitory histological structure including dying and replacement cells. At ED16, the folding of the IDE, which extended over the anterior two thirds of the molar, was the first sign of cuspidogenesis. It was accompanied by a local remodeling of the basement membrane (BM): IDE cells involved in this folding transitorily lost contact with the BM which formed a loop in the mesenchyme. During this period, the growth of the lower M1 along the antero-posterior axis was restricted to the posterior part of the molar. Histogenesis occurred in the whole EO, whilst initial cuspidogenesis was limited to the anterior part of the tooth. Distinct cell populations were thus involved in different contemporary processes leading to changes in the cell density in the mesenchyme, in the mitotic activity, in cell-shape, and cell-matrix interactions in the IDE, and remodeling of the BM where both epithelium and mesenchyme might participate.

Animals↗
PubMed1999

Alterations in the incisor development in the Tabby mouse.

The X-linked tabby (Ta) syndrome in the mouse is homologous to the hypohidrotic ectodermal dysplasia (HED) in humans. As in humans with HED, Ta mice exhibit hypohidrosis, characteristic defects of hairs and tooth abnormalities. To analyze the effects of Ta mutation on lower incisor development, histology, morphometry and computer-aided 3D reconstructions were combined. We observed that Ta mutation had major consequences for incisor development leading to abnormal tooth size and shape, change in the balance between prospective crown- and root-analog tissues and retarded cytodifferentiations. The decrease in size of Ta incisor was observed at ED13.5 and mainly involved the width of the tooth bud. At ED14.5-15.5, the incisor appeared shorter and narrower in the Ta than in the wild type (WT). Growth alterations affected the diameter to a greater extent than the length of the Ta incisor. From ED14.5, changes in the shape interfered with the medio-lateral asymmetry and alterations in the posterior growth of the cervical loop led to a loss of the labio-lingual asymmetry until ED17.0. Although the enamel organ in Ta incisors was smaller than in the WT, a larger proportion of the dental papilla was covered by preameloblasts-ameloblasts. These changes apparently resulted from reduced development of the lingual part of the enamel organ and might be correlated with a possible heterogeneity in the development of the enamel organ, as demonstrated for upper incisors. Our observations suggest independent development of the labial and lingual parts of the cervical loop. Furthermore, it appeared that the consequences of Ta mutation could not be interpreted only as a delay in tooth development.

Animals↗
PubMed1999

Morphogenesis of the lower incisor in the mouse from the bud to early bell stage.

The development of the lower incisor in the mouse was investigated from histological sections using computer-aided 3D reconstructions. At ED 13.0, the incisor was still at the bud stage. At ED 13.5, the initial cap was delimited by a short cervical loop, the development of which proceeded on the labial side, but was largely retarded on the medial side. This difference was maintained up to ED 15.0. From ED 16.0, the bell stage was achieved. Metaphases had a ubiquitous distribution both in the enamel organ and in the dental papilla from the bud to early bell stage. Apoptosis gradually increased in the mesenchyme posteriorly to the labial cervical loop from ED 13.5 to 14.0 and then disappeared; this apoptosis was not related to the posterior growth of the incisor. From ED 13.5, a high apoptotic activity was observed in the stalk. A focal area of apoptosis was observed at ED 13.5 in the enamel organ, approaching the epithelio-mesenchymal junction at the future tip of the incisor. There, the inner dental epithelium formed a bulbous protrusion towards dental papilla, reminiscent of the secondary enamel knot of mouse molars. This epithelial protrusion was still maintained at the bell stage. The enamel knot in the incisor demonstrated specific features, different from those characterizing the enamel knot in the molar: the concentric arrangement of epithelial cells was much less prominent and the occurrence of apoptosis was very transitory in the incisor at ED 13.5. The disappearance of the enamel knot despite a low apoptotic activity and the maintenance of the protrusion suggested a histological reorganization specific for rodent incisor.

Animals↗
PubMed1998

Correlation between apoptosis distribution and BMP-2 and BMP-4 expression in vestigial tooth primordia in mice.

The eutherian dental formula consists of three incisors, one canine, four premolars and three molars in each dental quadrant. Muroid evolution led to a reduction in the number of teeth, with one incisor separated from three molars by a long diastema. However, seven vestigial tooth primordia (D1-5, R1-2) have been detected in the embryonic diastemal area of the mouse maxilla between embryonic days (ED) 12.5 and 13.5. Computer-aided 3D reconstructions were used to analyse the temporo-spatial pattern of apoptosis during regression in the two largest and most distal vestiges (R1, R2). These structures have been widely considered as the primordium of the first upper molar and, accordingly, related molecular data have been interpreted exclusively in terms of progressive molar development. The spatial distribution of epithelial apoptosis, which affected the R1 and R2 rudiments in two consecutive waves on ED 12.5 and 13.5, respectively, was compared with our earlier data on expression of genes encoding bone morphogenetic proteins (BMP-2 and BMP-4). Similar temporo-spatial patterns of apoptosis and expression of BMP, specifically confined to the epithelium of the rudimentary tooth primordia, strongly support involvement of BMPs in the regulation of epithelial apoptosis during odontogenesis.

Animals↗
PubMed1998

Early stages of tooth morphogenesis in mouse analyzed by 3D reconstructions.

Computer-aided 3D reconstructions were used to investigate early odontogenesis in the ICR mouse, from the dental lamina to the cap stage. The diastemal region of the maxilla was not an empty zone: five transient epithelial rudiments (D1-D5) were found between ED 12.5-13.5. Two further rudiments (R1 and R2) were observed between D5 and the maxillary first molar primordium, whose bud emerged at ED 13.5. These rudiments might be related to vestiges of ancestral teeth. During this period, only an epithelial lamina was observed in front of the bud-shaped molar epithelium in the cheek region of the mandible. Apoptosis plays an important role in the reduction of antemolar rudiments in the maxilla and in the remodeling of the epithelium anterior to the M1 bud and cap in both jaws: two successive waves of apoptosis were detected in the mandible and in the maxilla. Computer-aided 3D reconstructions clearly demonstrated that morphologically different developmental stages coexist along the anteroposterior axis of M1 in both jaws.

Animals↗
PubMed1997

Cleft beak induced by hydrocortisone in the chick is prevented by increased cell division after experimental reduction of amniotic fluid.

Hypoplasia of the medial nasal process has been reported in chick embryos on embryonic day (ED) 5, 24 h after their exposure to hydrocortisone (HC). As a result, the cleft beak occurs in 80-100% of specimens on ED 9. In order to analyze its influence on cell proliferation, HC was injected intra-amniotically into embryos on ED 4, and the mitotic index and number of BrdU-positive cells were evaluated 24 h later, both in the epithelium and mesenchyme of the medial nasal processes, on serial frontal histological sections. Two hours after BrdU administration, there were 50% of labeled mesenchymal cells in the embryos exposed to HC and only 23% in the control group. The mitotic index of mesenchymal cells was significantly lower in the HC group than in the controls. The epithelium showed no significant difference. HC seemed to prevent the mesenchymal cells from entering mitosis. The cleft beak in the embryos exposed to HC on ED 4 was totally eliminated by tearing open the amnion (amniotomia) and allowing fluid to leak out on ED 5. In some of specimens exposed to HC, the mitotic index was investigated at six time intervals from 15 to 120 min after amniotomia. A significant increase in the mitotic index was detected in the mesenchymal cells of the medial nasal processes during the first hour after amniotomia. Such a prompt increase of the mitotic activity may be hypothetically explained by release of the HC from its receptor binding as a consequence of outflow of the amniotic fluid together with the HC pool, and freeing of the mesenchymal cells, blocked in the G2 phase, to enter mitosis. As a result, the hypoplasia of the medial nasal process might be compensated and the development of the cleft beak prevented.

Abnormalities, Drug-Induced↗
PubMed1997

Mouse molar morphogenesis revisited by three-dimensional reconstruction. III. Spatial distribution of mitoses and apoptoses up to bell-staged first lower molar teeth.

Computer-assisted 3D reconstructions were used to follow the development of the embryonic mouse first lower molar (M1). At ED 12.5, the thickening of the oral epithelium, which was thought to correspond to the molar dental lamina, regressed in its anterior part as a result of apoptosis. Only the posterior part later gave rise to molars. The transition to the cap stage entailed medial and lateral extensions of the dental epithelium. The growth and histo-morphogenesis of the enamel organ as well as cervical loop formation proceeded more rapidly in the anterior part of the M1 during the cap and early bell stages producing significant morphological differences along the antero-posterior axis. Apoptosis was temporarily intensive in the anterior part of the bud- and cap-shaped epithelium and thus pointed domains which do not participate in the formation of the final M1 enamel organ. In the well-formed cap, apoptoses displayed maximum concentration in the enamel knot (EK). No increase in the number of metaphases could be detected in the vicinity of the EK. Mitoses were distributed throughout the epithelial compartment until cap stage and then mainly concentrated in the inner dental epithelium at the early bell stage. At this later stage, either lateral views or thick virtual sections performed in the reconstruction demonstrated a clear cut distribution of mitoses and apoptoses in the enamel organ. At the early bell stage, mitoses in the mesenchyme demonstrated an increasing postero-anterior gradient.

Animals↗
PubMed1997

Different embryotoxic effect of vitamin A and B-carotene detected in the chick embryo.

Teratogenicity of vitamin A was firstly detected in experimental animals in 1953. Nearly 30 years later, teratogenicity of vitamin A analogue-isotretinoin was reported in humans. Isotretinoin induces serious birth defects of craniofacial and central nervous system, cardiovascular system and thymic malformations--in about 25% of babies exposed during the first trimester of their prenatal development. The biological interconversion of isotretinoin to vitamin A is known. That is why later epidemiological studies focused on high vitamin A intake in pregnant woman: Women who use daily vitamin A supplements during early pregnancy have approximately a two-fold increased risk of giving birth to a malformed baby. On the basis of these data, replacement of vitamin A has been recommended with its natural precursor B-carotene which is supposed to be more safe for pregnant woman due to its limited absorption from intestine. Aim of the present paper was to test a possible direct embryotoxic effect (i.e. lethality + teratogenicity) of B-carotene in chick embryos and to compare these results with known embryotoxicity of vitamin A in the same experimental model. Single subgerminal or intaamniotic injection of vitamin A or B-carotene within day 2-5 of incubation was used for estimation of the beginning of the embryotoxicity range determining the minimal embryotoxic doses. Vitamin A started to affect development between doses 0.3-0.3 microm [corrected] per embryo. Malformations of head, extremities and heart were detected similarly like in laboratory mammals and in man. B-carotene exhibited such an effect neither after injection of the highest tested doses-100 microm [corrected] per embryo. The results documented the strong difference in embryotoxicity between vitamin A and B-carotene. After theoretical extrapolation of the results achieved in the chick embryo, the minimal embryotoxic doses of vitamin A in mammals were estimated to be between 0.1-1 mg/kg of maternal weight and those of B-carotene to be more than 1000 mg/kg of maternal weight. Human epidemiological studies have proved teratogenicity of vitamin A after daily doses 25,000 i.u.-8.3 mg (0.13 mg/kg)- and reduction of its maximum intake has been recommended to 10,000 i.u. per day (0.05 mg/kg). The results about teratogenicity of vitamin A achieved in the chick embryo are in agreement with such a recommendation. Intake of vitamin A in the food is sufficient for pregnant woman in common Czech population. Therefore, an artificial supplementation of vitamin A brings risk of overdosage. If supplementation by vitamin A is unavoidable during pregnancy, B-carotene should be preferred.

Animals↗
PubMed1996

Timing of exchange of the maxillary deciduous and permanent teeth in boys with three types of orofacial clefts.

Timing of exchange of the deciduous and permanent maxillary teeth was investigated using dental plaster casts of 163 boys with total unilateral cleft (UCLP), 82 boys with bilateral cleft (BCLP), and 97 boys with isolated cleft palate (CP). All patients were treated at the Prague Plastic Surgery Clinic. The results were compared with a control group of 294 schoolboys. To evaluate the course of eruption, the proportion of each erupted teeth in each year of age was employed. In boys with UCLP, eruption of the permanent maxillary lateral incisors and the permanent maxillary second molar was retarded on the cleft side. On the non-affected side, no delay of eruption was observed, but earlier eruption was found in the permanent maxillary canine and in the permanent maxillary first and second premolars. In boys with BCLP, the highest retardation of eruption was found in the permanent maxillary lateral incisor and in the permanent maxillary first molar. The permanent maxillary canine and both permanent maxillary premolars erupted earlier than in the control group. In boys with CP, only the permanent maxillary central incisors erupted earlier. The maxillary deciduous canines and the second molars were both lost early. We conclude that the developmental disturbances of the maxillary jaw and teeth in patients with orofacial clefts are also associated with alteration of timing of dental exchange.

Adolescent↗
PubMed1996

Apoptosis is involved in the disappearance of the diastemal dental primordia in mouse embryo.

Three transient dental primordia (D1, D2 and D3) exist in the upper diastema in mouse embryos and their regression is associated with the presence of cell death. In order to specify the type of cell death and its temporo-spatial distribution, staining with hematoxylin, supravital staining with Nile Blue, TUNEL method, electron microscopic analysis and computer assisted 3-D reconstructions were performed. These data demonstrated that apoptosis is involved in the disappearance of the diastemal dental rudiments. Apoptosis occurred first with prevalence in the buccal part of the epithelium of the diastemal dental primordia and extended later to the whole epithelium of the dental rudiments and the dental lamina interconnecting them with the incisor and molar epithelia. Cell death occurred only sporadically in the adjacent mesenchyme. The prospective upper diastema in mouse embryos may provide a model for studies of developmental determination of toothless areas in the jaw as well as a tool for analyses of regulatory mechanisms of programmed cell death in morphogenesis.

Animals↗
PubMed1996

Sex differences in the incidence of orofacial clefts and the question of primary prevention in families with genetic risk.

Systematic registration of all children with orofacial clefts in Bohemia (Czech Republic) started at the Clinic of Plastic Surgery, Prague in 1964. A sample of 181 affected children with positive family histories (i.e. one of the parents had some type of orofacial cleft) was selected for the present study. The aim of this study was to follow the relation not only between the type of cleft in the child and in its parent, but also between the sex of the child and of the affected parent. Among children of mothers with cleft lip 68% were boys and only 32% were girls with cleft lip or cleft lip and palate. If the mother had cleft lip and palate, the same cleft type was found in 64% of boys and only 15% of girls. If the mother had cleft palate, the same cleft type was found in 37% of boys and 51% of girls. Very similar results were found for affected fathers and their children, with only one exception: among children of fathers with cleft lip and palate, the percentage of boys and girls with CLP was 43% and 40%, respectively. We can conclude that the cleft type in a child depends not only upon the cleft type present in the mother or father, but also upon the sex of the child. There was higher risk to have the orofacial cleft in sons of mothers with CL or CLP or fathers with CL and daughters of mothers or fathers with CP. The combination of the preconception choice of the sex of the baby with the ultrasonography method for the prenatal screening of malformations could decrease the risk delivering a child with an orofacial cleft in families with a genetic predisposition.

Child↗
PubMed1996

Mouse molar morphogenesis revisited by three dimensional reconstruction. I. Analysis of initial stages of the first upper molar development revealed two transient buds.

Early stages of tooth development in the maxillary cheek region in the mouse were investigated by combined analysis of histological sections, computer assisted 3D reconstructions and morphometry. In ED 12.5 embryos, 3D reconstructions revealed an accessory epithelial bud (R1) and a large bud (R2), which appeared as a single bud-shaped epithelium in frontal sections. This developmentally most advanced dental epithelium in the mouse embryonic maxilla until ED 13.5, generally considered as the bud of the first molar, regressed during later development. Meanwhile the bud and cap of the first upper molar originated more posteriorly, from ED 13.5. The regression of R1 and R2 was associated with epithelial apoptosis. Apoptotic cells and bodies were apparent on sections in the R1 epithelium from ED 12.5. The R2 epithelium maintained the large bud-shaped appearance on sections, representing the largest part of the dental epithelium in the maxillary cheek region until ED 14.0; apoptoses were detected there as late as from ED 13.5. During regression, the R2 rudiment was transformed into the medial and lateral epithelial ridges, posteriorly in continuity with the arising cap of the first molar. The reduced R1 epithelium seemed to contribute to the medial ridge. These results should be taken into consideration in the interpretation of early odontogenesis in the upper jaw in the mouse. The interesting problem of the identification of tooth homology of the rudiments should be elucidated by further comparative morphological and paleontological investigations.

Animals↗