Human adaptation in the 7th-11th century

This paper is an attempt to reconstruct human adaptability in the case of populations which lived in the central region of the Carpathian Basin between the 7th and 11th century. On drawing a parallel between the ecological zonality and the human anatomical patterns of the three historical periods included, we come to a conclusion that the populations of both the Late Avar period (670-894 A.D.) and the time of the Hungarian conquest (10th century, i.e. 895-999 A.D.) adapted themselves to the local ecological zonality fairly well, while, from 1000 A.D. on, i.e. at the time of the 11th century when the early Christian Hungarian Kingdom was founded by King St. Stephen, it may have been political intention more than anything else that influenced the structure of population

Váltóalapú likviditásteremtés

A kereskedelmi tevékenységből kifejlődő, a banki szféra által megerősített váltóhasználat napjainkra eltűnőben van, jóllehet gazdaságélénkítő ereje korábban a többi pénzügyi eszközhöz képest sokkal hatékonyabbnak bizonyult. Gazdaságtörténeti visszatekintéssel szeretnénk majd a két világháború közötti Németország sajátos pénzügypolitikai megoldását, a Hjalmar Schacht nevével fémjelzett modellt is elemezni a későbbiekben. Ennek célja annak idején – a költségvetési terhek növelése és infláció nélkül – a recesszióba zuhant német gazdaság beindítása volt. Az akkori cél, a speciális mennyiségi lazítással történő váltóalapú likviditásteremtés a 21. század megváltozott gazdasági-pénzügyi-intézményi keretei között még mindig érvényes tanulságokkal szolgálhat. A több évtizedes gazdaság-helyreállítási kísérletnek a megértéséhez szükséges, hogy a kétrészesre tervezett tanulmányunk első részében az állam által kezdeményezett váltóforgalmazás makrogazdasági összefüggéseit bemutassuk, majd pedig a vállalati szféra váltóhasználat általi megerősítési lehetőségének elemzésével foglalkozzunk. A likviditási nehézségek a hazai gazdasági szereplők pénzügyi mozgásterét igen beszűkítik, a tanulmányunk ezen részében javaslatokat teszünk a váltóforgalmazással megvalósítható fejlesztésekre. Journal of Economic Literature (JEL) kód: G18, G21, G32

Az autochtonitás hatása az Alföld honfoglalás kori (10. századi) népességére

The present paper deals with the 10th century population history of the Hungarian Great Plain. Our attention was primarily focused on the proportion of the 10th century Hungarian conquerors and the local populations. As the craniological results showed, the percentage of the local population might have been 57%, while that of the immigrants might have presented a smaller ratio (43%). The components of the local population were also estimated back to the previous one thousand years. According to these examinations, the characteristic features of the population surviving in the Great Plain were mainly suggestive of the Sarmatian and Germanic eras. The immigrants of the Late Avar period preceding the age of the Hungarian conquest did not seem to have been of the same importance

Hemokinin-1 Gene Expression Is Upregulated in Trigeminal Ganglia in an Inflammatory Orofacial Pain Model: Potential Role in Peripheral Sensitization

A large percentage of primary sensory neurons in the trigeminal ganglia (TG) contain neuropeptides such as tachykinins or calcitonin gene-related peptide. Neuropeptides released from the central terminals of primary afferents sensitize the secondary nociceptive neurons in the trigeminal nucleus caudalis (TNC), but also activate glial cells contributing to neuroinflammation and consequent sensitization in chronic orofacial pain and migraine. In the present study, we investigated the newest member of the tachykinin family, hemokinin-1 (HK-1) encoded by the Tac4 gene in the trigeminal system. HK-1 had been shown to participate in inflammation and hyperalgesia in various models, but its role has not been investigated in orofacial pain or headache. In the complete Freund's adjuvant (CFA)-induced inflammatory orofacial pain model, we showed that Tac4 expression increased in the TG in response to inflammation. Duration-dependent Tac4 upregulation was associated with the extent of the facial allodynia. Tac4 was detected in both TG neurons and satellite glial cells (SGC) by the ultrasensitive RNAscope in situ hybridization. We also compared gene expression changes of selected neuronal and glial sensitization and neuroinflammation markers between wild-type and Tac4-deficient (Tac4-/-) mice. Expression of the SGC/astrocyte marker in the TG and TNC was significantly lower in intact and saline/CFA-treated Tac4-/- mice. The procedural stress-related increase of the SGC/astrocyte marker was also strongly attenuated in Tac4-/- mice. Analysis of TG samples with a mouse neuroinflammation panel of 770 genes revealed that regulation of microglia and cytotoxic cell-related genes were significantly different in saline-treated Tac4-/- mice compared to their wild-types. It is concluded that HK-1 may participate in neuron-glia interactions both under physiological and inflammatory conditions and mediate pain in the trigeminal system

Az indvidualizált farmakoterápia lehetőségének kidolgozása - súlyos bőrgyógyászati mellékhatásokkal is járó adverz gyógyszerreakciók farmakogenomikai és etiológiai vizsgálata, genetikai megelőzése, preventív rendszerek, tesztek fejlesztése = Working towards the realization of personalized medicine - pahrmacogenomic and etiological study of adverse drug reactions with severe cutan involvement, developing preventive systems and assays

Pharmacogenomika: 80 lamotrigint vagy carbamazepint szedő beteg- súlyos cután gyógyszermellékhatással vagy a nélkül adatait és DNS-ét archiváltuk. A DNS mintákat CYP2D6 és CYP2C19 polymorphismusra Amplichip CYP450 IVD kittel Affymetrix Gene Chip Fluidics Station 450-en és/vagy Affymetrix Drug Metabolizing Enzymes and Transporters (DMET+) rendszerben vizsgáltuk. 4 technikai probléma- prolongált vizsgálat: 1, Az első mérések elavult software-t jeleztek, cseréltük 2. Ez új 7G reading chip rendszert igényelt. A 4 állomásból 3 működik 3, A két Roche teszt-chip lejárt kóddal érkezett 4, Előzetes génvizsgálatokat kezdtük az Affymetrix Genotyping Console software-rel, DMET chipeken, de a releváns eredmények PCR re-tesztelése most zajlik. További vizsgálatok Állati eredetű anabolikus steroidok és fokozott aminosav bevitele volt a kiváltó faktor eosinophil fasciitises testépítő betegünkben,akiben a készítmények alkalmazását követően új, állati eredetű mycoplasma arginini fertőzést igazoltunk. Súlyos gyógyszermellékhatásban szenvedő betegeinket teszteltünk társuló mycoplasma infekciókat PCR-rel és szerológiai módszerekkel. Bevezettük az epicutan gyógyszertesztelést tünetmentes betegeinkben. Atomerőműben szűrtünk bőrdaganatokat- szabadidős UV expozíció hatását igazoltuk- (fényérzékenyítő gyógyszereket nem szedtek). Két magyar összefoglaló tanulmány: 1, Toxicodermákban végzett LTT tesztek eredményéről 2, Erythema multiformében a gyógyszermellékhatásgyakoriságáról. | Pharmacogenomics: data and DNA from 80 patients under lamotrigine or carbamazepine therapy with or without severe cutaneous adverse effects were collected. DNAs were analyzed for CYP2D6 and CYP2C19 polymorphisms by Amplichip CYP450 IVD kit on an Affymetrix Gene Chip Fluidics Station 450 and by Affymetrix Drug Metabolizing Enzymes and Transporters (DMET + Solution) chip. 4 problems - study prolongation. 1, Uncertain data indicated an old software system, the change needed new 7G reading chips in our Affymetrix Station. 2,Still, one out of 4 stations is not working currently 3, Two Roche test chips arrived by expired codes 4, Preliminary genetic studies were also performed by an Affymetrix Genotyping Console software on a DMET chip and relevant genes and polymorphisms are currently under PCR re-testing. Further studies In a patient with eosinophil fasciitis induced by anabolic steroid and aminoacid intake from uncontrolled animal sources we identified a new animal mycoplasma arginini infection. In patients severe drug adverse reactions associated mycoplasma infections were studied by PCR and immunology. We introduced the patch testing for drug sensitivity. In a Hungarian nuclear power plant screened for cutaneous malignancies the role of outdoor UV was identified - without drug induced photosensitivity. Hungarian papers on lymphocyte transformation drug testing and erythema multiforme also related to drug sensitivity were published

A kórokozó és a gazdaszervezet kölcsönhatásának immunológiai befolyásolása

In this thesis we have reviewed the scientific literature related to the subject matters of our work. We have briefly summarized the literature of the innate immune response focusing on the research related to pathogen recognition. These include the Toll-like receptors (TLR) and other pathogen recognition receptors (PRR). We have also reviewed the literature of dendritic cells (DC) with the focus on the pathogen recognition receptor, dendritic cell specific ICAM grabbing non-integrin (DC-SIGN) and the roles of dendritic cell TLRs in induction of Th1 helper response. In addition, we reviewed briefly the literature of the particle based carrier systems as well as the interaction of mycoplasmas with TLRs and M. gallisepticum (MG) infection. In Experiment 1, we described the removal of a TLR-4 agonist molecule, endotoxin, from different solutions using affinity technology. The endotoxin concentrations were measured using the Limulus Amoebocyte Lysate (LAL) assay. We have demonstrated endotoxin binding from water, Pseudomonas supernatant, and sa(lt solutions by spiking the samples with known amounts of endotoxin. We have tested the reusability of the affinity resin by cleaning it with NaOH as well as hot water sanitization. Leachables from the affinity resin that could potentially contaminate the solutions were also tested for. We have also investigated if the resin changed the composition of the salt solution. In Experiment 2, we have described the removal of TLR agonist molecules, such endotoxin (TLR-4), peptidoglycan (TLR-2/Nod2), lipopeptide (TLR-2) and bacterial DNA (TLR-9) from blood and plasma using affinity technology. We have tested the efficacy of removal by spiking the anti-coagulated blood and plasma with known amount of TLR agonist and measured their capture under dynamic conditions. We have tested several affinity resins, and the result of the most efficient one is presented here. The removal of endotoxin was tested with the LAL assay, while we have used monocyte activation assay (TNF-α ELISA) for testing the removal of the other TLR agonist molecules. Tissue Factor (TF) assay was used to determine the effect of the removal of TLR agonists on the coagulation part of the innate immune system. We have tested that the affinity resin, while removing the TLR agonist molecules does not have a negative effect on the blood by assaying the parameters of the coagulation, complement activation, hemolysis and cell count. In Experiment 3, we have described mycoplasma capture from solutions, such as serum used in cell culture, by affinity technology. We have used serologically and biochemically different mycoplasmas and affinity resins that are specific for different lipid and carbohydrate moieties on the mycoplasma membranes. In Experiment 4, we have described synergistic effect of TLR agonist molecules, such as peptidoglycan (TLR-2/Nod2) and bacterial DNA (TLR-9) on the stimulation of the innate immune response. Monocyte culture-based activation assay for tumor necrosis factor-αTNF-α and Tissue Factor levels (ELISA) were used to demonstrate their effect. We have also determined the effective concentrations of these TLR agonists that synergistically induce TNF-α and Tissue Factor production. In Experiment 5, we have described the preparation of pathogen mimicking microparticles, which included the preparation of an immunoaffinity column using purified polyclonal antibodies from a M. gallisepticum-positive sera, the immunoaffinity purification of M. gallisepticum antigens and the biochemical modification of the antigens (Endoglycosidase H (EndoH) digestion, Concanavalin A (ConA) adsorption, periodate oxidization and deacylation). In addition we have described the immobilization of antigens and PRR agonists, such as TLR-2, TLR-3, TLR-4, TLR-9 and nucleotid oligomerization domain 2 (Nod2) agonists to the microparticles. These microparticles are used in vivo (Experiment 6) and in vitro (Experiment 7). In Experiment 6, we have used a M. gallisepticum challenge model in chickens to test the effect of the pathogen mimicking microparticles. We have set up test groups of chickens (10 chickens per group) that were treated with the immunomodulatory microparticles orally 14 days prior to the M. gallisepticum challenge or after the challenge. The chickens were challenged with M. gallisepticum Rlow, a highly pathogenic strain of M. gallisepticum. Fourteen days after the challenge, the chickens were euthanized and examined for pathological lesions. Samples from different organs were taken for culture for M. gallisepticum as well as histopathology. In the challenge experiment, we have examined and compared the effects of PRR agonists, M. gallisepticum and M. gallinarum membranes, and the immunoaffinity-purified antigens with or without PRR agonist molecules. We have also examined the effect of the different post-transcriptional modifications of the M. gallisepticum antigens on the immune response. In Experiment 7, we have used the pathogen mimicking microparticles to study their effect in vitro with peripheral blood mononuclear cells (PBMC) and dendritic cells. We have induced monocytes with IL-4 and GM-CSF (granulocyte, macrophage colony stimulating factor) to obtain dendritic cells. We have been able to demonstrate that the microparticles interact with the cells of the innate immune system, such as PBMC and dendritic cells. We have assayed the activation of these cells by testing the level of pro-inflamatory cytokine, TNF-α and anti-inflamatory cytokine, IL-10 induction using ELISA. We have labeled the microparticles with fluorescein and used flow cytometry to show interaction with dendritic cells. We have shown that the microparticles used as an immunomodulator induce changes that are hallmarks of dendritic cells maturation, such as increase in the expression of MHCII (major histocompatibility complex) molecules and CD86 molecules. These were assayed by flow cytometry. Since the dendritic cells are the link between the innate and adaptive immunity, we have been able to show that the microparticles are able to influence both the innate and adaptive immune response