Results of the paleostomatological researches

Hungarian paleostomatology as the part of dental anthropology exists since the middle of the last century, together with the paleodontical research in the world. The name paleostomatology comes from a Hungarian scientist, György Huszár. The article has the following chapters: Introduction (what is paleostomatology, and its importance), First studies in the world, Nomenclature, The bases of Hungarian paleostomatology, Pioneers of paleostomatological studies in Hungary, Era of the study of caries and other fields of Hungarian paleostomatology, and Hungarian paleostomatology today. The most important representatives of the field are Árkövy, Bruszt, Hillebrand, Huszár, Iszlai, M Lenhossék, Schranz, Tóth, and many anthropologists, doctors, dentists and other scientists. The most researched topics are dental morphology and dental caries but the scientists deal with other fields, too, from an anthropological or medical point of view, such as the morphology and pathology of the facial bones, the alveolar changes, the tooth morphology and variations, the developmental anomalies, the dental attrition, the articulation of dentitions, and so on. In the last couple of years the level of methodology have also corresponded to international needs

Supernumerary occlusal cusps on permanent human teeth

Supernumerary (central) cusps that appear on the occlusal surface of the teeth have already been grouped by many authors. The most comprehensive grouping of central cusps on the premolars is that by Schulze (1987). However, different central cusp forms may occur on the molar teeth, and cusp-like protrusions may also develop on the incisors and the canines. In the present work, plaster casts of the teeth of 500 orthodontic patients (250 males and 250 females) were examined for central cusps at the above departments. The central cusps appeared on the dentition of 47.6% of the investigated Hungarian population . From a total of 13,79 3 teeth examined , 501 (3.69% ) were observed to display a central cusp. The teeth most often affected were the mandibular first premolars (11.6%). A new central cusp form , the "margoid central cusp formation," was noted

Foghiányokat kísérő egyszerű nukleotid polimorfizmusok hypodontiában = Single nucleotide polymorphisms in hypodontia

Komplex megközelítéssel tanulmányoztuk a fogcsírahiányban feltehetőleg résztvevő több egyszerű nukleotid polimorfizmust (SNP) a magyar populációban. A PAX9, az MSX1, az FGFR1, az IRF6 és az AXIN2 nyolc polimorfizmusát vizsgáltuk 192 hipodonciás, 17 oligodonciás és 260 egészséges önkéntes esetében. Az eset-kontroll analízisben mind az allél, mind a genotípus asszociációk gyakoriságát, valamint a haplotípus szintű asszociációk gyakoriságát tanulmányoztuk. Többváltozós Bayes hálózat alapú többszintű valószínűségi analízist (BN-BMLA) és logisztikus regressziót végeztünk. A hagyományos statisztikák azt mutatták, hogy a PAX9 -912-es SNP és az MSX1 SNP megváltoztatta a hipodoncia előfordulását, de korrekció után a hatások csak marginális tendenciát mutattak. A többszörös hipotézis tesztelésre alkalmasabb BN-BMLA analízist használva a PAX9 SNP-k szinergikus hatást adtak. Ezt megerősítette más többváltozós analízis is, és az összefüggés szignifikáns maradt a többszörös hipotézis tesztelés után is . A PAX9-1031-A-PAX9-912-T haplotípus volt a legjelentősebb kombináció ami csírahiányt okozott. PAX9 és MSX1 között az együtthatás gyengébb volt, míg más SNP-nek nem volt hatása a hipodonciára. Komplex analízisünk megmutatta a PAX9 és MSX1-es SNP-k együtthatásának fontos szerepét a fogcsírahiányra, míg az IRF6, FGFR1 és Axin2 SNP-knek nem volt detektálható szerepe a magyar populációban. A mi eredményeink is rávilágítanak a populációk közötti eltérések jelentőségére. | We studied the role of multiple single nucleotide polymorphisms (SNP) in tooth agenesis in the Hungarian population using a complex approach. Eight SNPs of PAX9, MSX1, FGFR1, IRF6 and AXIN2 were studied in 192 hypodontia and 17 oligodontia cases and in 260 healthy volunteers. Case-control analysis was performed to test both allelic and genotypic associations as well as associations at the level of haplotypes. Multivariate exploratory Bayesian network based multilevel analysis of relevance (BN-BMLA) as well as logistic regression analysis were performed. Conventional statistics showed that PAX9 SNP -912 C/T and the MSX1 SNP changed the incidence of hypodontia, although after correction the effects were only borderline tendencies. Using a statistical analysis better suited for handling multiple hypotheses, the BN-BMLA, PAX9 SNPs clearly showed a synergistic effect. This was confirmed by other multivariate analyses and it remained significant after corrections for multiple hypothesis testing. The PAX9-1031-A-PAX9-912-T haplotype was the most relevant combination causing hypodontia. Interaction was weaker between PAX9 and MSX1, while other SNPs had no joint effect on hypodontia. Our complex analysis shows the important role of PAX9 and MSX1 SNPs and of their interactions in tooth agenesis, while IRF6, FGFR1 and AXIN2 SNPs had no detectable role in the Hungarian population. Our results also reveal the variations of risk factors in hypodontia

Cleavage of Kininogen and Subsequent Bradykinin Release by the Complement Component: Mannose-Binding Lectin-Associated Serine Protease (MASP)-1

Bradykinin (BK), generated from high-molecular-weight kininogen (HK) is the major mediator of swelling attacks in hereditary angioedema (HAE), a disease associated with C1-inhibitor deficiency. Plasma kallikrein, activated by factor XIIa, is responsible for most of HK cleavage. However other proteases, which activate during episodes of angioedema, might also contribute to BK production. The lectin pathway of the complement system activates after infection and oxidative stress on endothelial cells generating active serine proteases: MASP-1 and MASP-2. Our aim was to study whether activated MASPs are able to digest HK to release BK. Initially we were trying to find potential new substrates of MASP-1 in human plasma by differential gel electrophoresis, and we identified kininogen cleavage products by this proteomic approach. As a control, MASP-2 was included in the study in addition to MASP-1 and kallikrein. The proteolytic cleavage of HK by MASPs was followed by SDS-PAGE, and BK release was detected by HPLC. We showed that MASP-1 was able to cleave HK resulting in BK production. MASP-2 could also cleave HK but could not release BK. The cleavage pattern of MASPs is similar but not strictly identical to that of kallikrein. The catalytic efficiency of HK cleavage by a recombinant version of MASP-1 and MASP-2 was about 4.0×102 and 2.7×102 M−1s−1, respectively. C1-inhibitor, the major inhibitor of factor XIIa and kallikrein, also prevented the cleavage of HK by MASPs. In all, a new factor XII- and kallikrein-independent mechanism of bradykinin production by MASP-1 was demonstrated, which may contribute to the pro-inflammatory effect of the lectin pathway of complement and to the elevated bradykinin levels in HAE patients

Median raphe region stimulation alone generates remote, but not recent fear memory traces

The median raphe region (MRR) is believed to control the fear circuitry indirectly, by influencing the encoding and retrieval of fear memories by amygdala, hippocampus and prefrontal cortex. Here we show that in addition to this established role, MRR stimulation may alone elicit the emergence of remote but not recent fear memories. We substituted electric shocks with optic stimulation of MRR in C57BL/6N male mice in an optogenetic conditioning paradigm and found that stimulations produced agitation, but not fear, during the conditioning trial. Contextual fear, reflected by freezing was not present the next day, but appeared after a 7 days incubation. The optogenetic silencing of MRR during electric shocks ameliorated conditioned fear also seven, but not one day after conditioning. The optogenetic stimulation patterns (50Hz theta burst and 20Hz) used in our tests elicited serotonin release in vitro and lead to activation primarily in the periaqueductal gray examined by c-Fos immunohistochemistry. Earlier studies demonstrated that fear can be induced acutely by stimulation of several subcortical centers, which, however, do not generate persistent fear memories. Here we show that the MRR also elicits fear, but this develops slowly over time, likely by plastic changes induced by the area and its connections. These findings assign a specific role to the MRR in fear learning. Particularly, we suggest that this area is responsible for the durable sensitization of fear circuits towards aversive contexts, and by this, it contributes to the persistence of fear memories. This suggests the existence a bottom-up control of fear circuits by the MRR, which complements the top-down control exerted by the medial prefrontal cortex