[et_pb_section fb_built=”1″ _builder_version=”3.22.7″ custom_padding=”||5px|||”][et_pb_row _builder_version=”3.25″][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_text _builder_version=”4.6.6″]<\/p>\n
[\/et_pb_text][\/et_pb_column][\/et_pb_row][\/et_pb_section][et_pb_section fb_built=”1″ specialty=”on” _builder_version=”3.22.3″ custom_padding=”24px|0px|25px|0px|false|false”][et_pb_column type=”3_4″ specialty_columns=”3″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_row_inner _builder_version=”3.25″][et_pb_column_inner saved_specialty_column_type=”3_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_blurb title=”Editoral in Hungarian ” url=”https:\/\/mppt.hu\/magazin\/pdf\/xiii-evfolyam-1-szam\/szerk.%20rethelyi%20web.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xiii-evfolyam-1-szam\/szerk. rethelyi web.pdf” link_option_url_new_window=”on”]<\/p>\n
J\u00e1nos R\u00e9thelyi<\/p>\n
[\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”4.6.6″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n
A glutam\u00e1t, az agyban legnagyobb koncentr\u00e1ci\u00f3ban el\u0151fordul\u00f3 excit\u00e1toros neurotranszmitter receptorai k\u00f6z\u00e9 tartozik az N-metil-D-aszpart\u00e1t (NMDA) receptor. Mint ismeretes, az NMDA-neurtranszmisszi\u00f3 sz\u00e1mos fiziol\u00f3gi\u00e1s neurobiol\u00f3giai folyamatban \u00e9s agyi betegs\u00e9gben j\u00e1tszik fontos szerepet. A molekul\u00e1ris pszichi\u00e1triai kutat\u00e1sok \u00e9s a mindennapi klinikusi m\u0171k\u00f6d\u00e9s szempontj\u00e1b\u00f3l is \u00e9rdemes \u00e1ttekintenu\u0308nk az elm\u00falt egy-k\u00e9t \u00e9v \u00faj eredm\u00e9nyeit az NMDA-receptorrendszerrel kapcsolatban. (A t\u00e9m\u00e1val kapcsolatban kit\u0171n\u0151 \u00f6sszefoglal\u00e1sok olvashat\u00f3k magyar \u00e9s angol nyelven is: Horv\u00e1th \u00e9s mtsai, 2009; Paoletti \u00e9s Neyton, 2007; Wikipedia, 2011.)<\/span><\/p>\n Az ionotr\u00f3p glutam\u00e1t receptor nev\u00e9t specifikus agonist\u00e1j\u00e1r\u00f3l, az N-metil-D-aszpart\u00e1t molekul\u00e1r\u00f3l kapta, amely csak ehhez a receptort\u00edpushoz k\u00f6t\u0151dik. A receptor aktiv\u00e1ci\u00f3j\u00e1nak eredm\u00e9nye egy nonszelekt\u00edv, a sejtmembr\u00e1non \u00e1t\u00edvel\u0151 ioncsatorna megny\u00edl\u00e1sa. A tetramer, n\u00e9gy alegys\u00e9gb\u0151l \u00e1ll\u00f3 feh\u00e9rje extracellul\u00e1ris, transzmembr\u00e1n \u00e9s citoplazmatikus dom\u00e9nekb\u0151l \u00e1ll. Alternat\u00edv splicing r\u00e9v\u00e9n sz\u00e1mos receptor izoforma expressz\u00e1l\u00f3dik az agy ku\u0308l\u00f6nb\u00f6z\u0151 teru\u0308letein. Az NR1 alegys\u00e9g extracellul\u00e1ris r\u00e9sz\u00e9hez k\u00f6t\u0151dik a receptor koagonist\u00e1ja, a glicin molekula, m\u00edg az NR2 alegys\u00e9g extracellul\u00e1ris r\u00e9sz\u00e9n tal\u00e1lhat\u00f3 a glutam\u00e1tot vagy aszpart\u00e1tot k\u00f6t\u0151 hely. A glicin k\u00f6t\u0151d\u00e9s\u00e9nek alloszterikus modul\u00e1tora a d-szerin. Az intracellul\u00e1ris dom\u00e9n m\u00e1s v\u00e1zfeh\u00e9rj\u00e9khez k\u00f6t\u0151dik. Az NMDA-receptorok k\u00e9t szempontb\u00f3l is egyediek, egyr\u00e9szt az aktiv\u00e1ci\u00f3jukhoz egyar\u00e1nt szu\u0308ks\u00e9g van mindk\u00e9nt ligand, a glutam\u00e1t \u00e9s a glicin k\u00f6t\u0151d\u00e9s\u00e9re. M\u00e1sr\u00e9szt a receptor egyar\u00e1nt ligand- \u00e9s feszu\u0308lts\u00e9gfu\u0308gg\u0151, ez azt jelenti, hogy a ligandok k\u00f6t\u0151d\u00e9se mellett is csak a neuron m\u00e1s ioncsatorn\u00e1kon (p\u00e9ld\u00e1ul alfa-amino-3-hidroxi-5-metilizoxazol- 4-proprionsav, AMPA) t\u00f6rt\u00e9n\u0151 depolariz\u00e1ci\u00f3ja ut\u00e1n ny\u00edlik meg az NMDA-receptor transzmembr\u00e1n r\u00e9sze, az extracellul\u00e1risan elhelyezked\u0151 magn\u00e9zium-ionok kil\u00f6k\u0151d\u00e9se r\u00e9v\u00e9n.<\/p>\n A receptor ez ut\u00f3bbi tulajdons\u00e1ga \u2013 hogy egyszerre ligand- \u00e9s feszu\u0308lts\u00e9gfu\u0308gg\u0151 \u2013 teszi alkalmass\u00e1 a mem\u00f3ri\u00e1ban, tanul\u00e1sban, szinaptikus plaszticit\u00e1sban bet\u00f6lt\u00f6tt szerep\u00e9re. A postszinaptikus membr\u00e1n Mi\u00e9rt fontos mindez sz\u00e1munkra? Az NMDA-rendszer t\u00falm\u0171k\u00f6d\u00e9se excitotoxicit\u00e1st okoz, amelynek Pszichofarmakol\u00f3giai szempontb\u00f3l is fontos elm\u00e9lyednu\u0308nk az NMDA-rendszerben. Az Alzheimerdemenci\u00e1ban haszn\u00e1lt memantin, amely nem kompetit\u00edv NMDA-antagonista, cs\u00f6kkenti az excitotoxicit\u00e1s el\u0151fordul\u00e1s\u00e1t, ugyanakkor nem blokkolja a norm\u00e1lis glutam\u00e1terg neurotranszmisszi\u00f3t. Az alkohol-betegs\u00e9gben probl\u00e9m\u00e1t jelent\u0151 s\u00f3v\u00e1rg\u00e1s m\u00e9rt\u00e9k\u00e9t cs\u00f6kkenti az acamprosate, amely szint\u00e9n az alkoholizmusban felu\u0308lregul\u00e1lt NMDA-receptorok t\u00falzott m\u0171k\u00f6d\u00e9s\u00e9t cs\u00f6kkenti. Izgalmas eredm\u00e9ny a k\u00f6zelm\u00faltb\u00f3l, hogy szkizofr\u00e9n betegekben nagy d\u00f3zis\u00fa (60-120 mg) d-szerin antipszichotikus ter\u00e1pia melletti ad\u00e1s\u00e1val szignifik\u00e1ns, k\u00f6zepest\u0151l nagyig terjed\u0151 hat\u00e1sm\u00e9retet jelent\u0151 javul\u00e1s volt el\u00e9rhet\u0151 a negat\u00edv tu\u0308netekben \u00e9s a kognit\u00edv funkci\u00f3kban (Kantrowitz \u00e9s mtsai, 2010). Hab\u00e1r a k\u00f6vetkez\u0151 fejlem\u00e9ny az NMDA-receptorrendszeren m\u00e1r t\u00falmutat, fontos figyelemmel k\u00eds\u00e9rnu\u0308nk, hogy t\u00f6bb molekul\u00e1val \u2013 melyek a glutam\u00e1t m\u00e1sik t\u00edpus\u00fa, metabotr\u00f3p receptorainak agonist\u00e1i vagy modul\u00e1torai \u2013 zajlanak preklinikai vagy klinikai vizsg\u00e1latok, mint potenci\u00e1lis antipszichotikumokkal (Snyder \u00e9s Murphy, 2008). K\u00e9rd\u00e9s, hogy \u00e9ppen a glutam\u00e1terg neurotranszmisszi\u00f3 nagyfok\u00fa agyi elterjedts\u00e9ge miatt hat\u00e9konynak \u00e9s toler\u00e1lhat\u00f3nak bizonyulnak-e ezek az \u00faj molekul\u00e1k.<\/p>\n \u00d6sszefoglalva: Az NMDA-rendszer m\u00e9g sok \u00fajdons\u00e1got tartogat sz\u00e1munkra. \u00c9rdemes odafigyelni r\u00e1.<\/p>\n<\/div>\n [\/et_pb_toggle][et_pb_blurb title=”Genetic and pharmacogenomic data on smoking: the bigger sample size, the less reliable phenotype? A critical review” url=”https:\/\/mppt.hu\/magazin\/pdf\/xiii-evfolyam-1-szam\/lazry%20web.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xiii-evfolyam-1-szam\/lazry web.pdf” link_option_url_new_window=”on”]<\/p>\n Judit Lazary, Peter Dome and Gabor Faludi<\/p>\n [\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”3.22.7″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n <\/p>\n<\/div>\n Increasing amount of genetic data on nicotine dependence (ND) is available in the literature, sometimes extremely large population size is reported but the study design is not always consequent. Phenotypic measures can vary from a simple 6-item self-rating scale to breath CO or serum cotinine level test but in genetic investigations this is not sophisticated; moreover the population stratification is also usually ignored. In contrast, possibly because of the strict traditions of pharmacological investigations, pharmacogenomic studies on smoking cessation therapy use more reliable phenotypic measures with high quality design consequently involving fewer participants. In spite of the heavy epidemiological data on smoking in Hungary, genetic background of heavy smoking is still not studied in this population. In this review we sum up the most important, replicated results but we also provide some critical remarks about the methodological shortcomings of these studies. Keeping in mind the value of large scale population ND association studies we would also like to emphasize that the clinical implementation of studies with larger samples but with weaker methodology and statistical analyses is limited. Similar to many other psychiatric disorders, ND is a multifactorial condition, therefore the measure of genetic effects requires a more complex study design.\u00a0<\/p>\n Keywords:<\/strong>\u00a0smoking, nicotine dependence, pharmacogenomics, smoking-related phenotypes, genetic epidemiological studies<\/p>\n<\/div>\n [\/et_pb_toggle][et_pb_blurb title=”Nanomedicine: Application of Nanotechnology in Medicine. Opportunities in Neuropsychiatry” url=”https:\/\/mppt.hu\/magazin\/pdf\/xiii-evfolyam-1-szam\/szebeni%20web.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xiii-evfolyam-1-szam\/szebeni web.pdf” link_option_url_new_window=”on”]<\/p>\n J\u00e1nos Szebeni<\/p>\n [\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”3.22.7″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n One of the most popular, most intensely expanding borderline of science and technology Keywords<\/strong>: nanotherapy, nanocarriers, targeted pharmacotherapy, liposomes, neuropsychopharmacons, blood-brain barrier<\/p>\n<\/div>\n [\/et_pb_toggle][et_pb_blurb title=”Neurocognition and psychogenetic vulnerability in depression” url=”https:\/\/mppt.hu\/magazin\/pdf\/xiii-evfolyam-1-szam\/sarosi%20web.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xiii-evfolyam-1-szam\/sarosi web.pdf” link_option_url_new_window=”on”]<\/p>\n Andrea Sarosi<\/p>\n [\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”3.22.7″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n The clinical symptoms of major depression are paralleled by typical neurocognitive deficits. The relation of STin2 – one of the polymorphisms of the serotonin transporter gene – to major depressive disorder (MDD) is less widely investigated. The aim of the present study was to measure the neurocognitive functions of major depressive patients and healthy controls, and identify vulnerability markers of the disease. The frequency of STin2 polymorphism and its effect on neurocognition was investigated in major depression. The gender differences in neurocognitive impairment in patients with major depressive disorder were also studied. Relative to controls, patients with depression showed significant impairment on most neurocognitive tasks, but not in tasks measuring visuo-spatial function, which may suggest intact hippocampal function in depression. We found a significantly higher frequency of the STin2 10\/10 genotype in the MDD patient group compared to controls. Our results suggest that the presence of STin2.10 and absence of STin2.12 may be considered a possible genetic endophenotype for cognitive dysfunction detected in major depressive disorder. Depressed women performed significantly worse on tests of cognitive interference and visual recall threshold compared to depressed men. In the light of neuroimaging studies our results suggest that the lateralisation of hippocampal function may play an important role in the background of gender differences.<\/p>\n Keywords:<\/strong>\u00a0depression, neurocognition, cognitive dysfunction, vulnerability marker, serotonin transporter, STin2 polymorphism, endophenotype, gender difference<\/p>\n<\/div>\n [\/et_pb_toggle][et_pb_blurb title=”Evaluation of the psychometric properties of the Calgary Depression Scale for Schizophrenics (CDSS) in a Hungarian clinical population of patients with schizophrenia” url=”https:\/\/mppt.hu\/magazin\/pdf\/xiii-evfolyam-1-szam\/nagy%20judit%20web.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xiii-evfolyam-1-szam\/nagy judit web.pdf” link_option_url_new_window=”on”]<\/p>\n Judit \u00a0Nagy and Istv\u00e1n\u00a0Bitter<\/p>\n [\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”3.22.7″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n Objective: Evaluation of the reliability and validity of the Hungarian version of the Calgary Keywords<\/strong>: Calgary Depression Scale for Schizophrenia, validity, reliability, Hungarian version, [\/et_pb_toggle][\/et_pb_column_inner][\/et_pb_row_inner][\/et_pb_column][et_pb_column type=”1_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_image src=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/05\/2011-marcius-borito-1.png” align_tablet=”center” align_phone=”” align_last_edited=”on|desktop” _builder_version=”3.23.3″ box_shadow_style=”preset3″][\/et_pb_image][\/et_pb_column][\/et_pb_section]<\/p>\n","protected":false},"excerpt":{"rendered":" VOLUME 13, ISSUE 1, MARCH 2011J\u00e1nos R\u00e9thelyiA glutam\u00e1t, az agyban legnagyobb koncentr\u00e1ci\u00f3ban el\u0151fordul\u00f3 excit\u00e1toros neurotranszmitter receptorai k\u00f6z\u00e9 tartozik az N-metil-D-aszpart\u00e1t (NMDA) receptor. Mint ismeretes, az NMDA-neurtranszmisszi\u00f3 sz\u00e1mos fiziol\u00f3gi\u00e1s neurobiol\u00f3giai folyamatban \u00e9s agyi betegs\u00e9gben j\u00e1tszik fontos szerepet. A molekul\u00e1ris pszichi\u00e1triai kutat\u00e1sok \u00e9s a mindennapi klinikusi m\u0171k\u00f6d\u00e9s szempontj\u00e1b\u00f3l is \u00e9rdemes \u00e1ttekintenu\u0308nk az elm\u00falt egy-k\u00e9t \u00e9v \u00faj eredm\u00e9nyeit […]<\/p>\n","protected":false},"author":4,"featured_media":49655,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_et_pb_use_builder":"on","_et_pb_old_content":"","_et_gb_content_width":"","footnotes":""},"project_category":[64],"project_tag":[],"class_list":["post-49470","project","type-project","status-publish","has-post-thumbnail","hentry","project_category-2011-en"],"_links":{"self":[{"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project\/49470","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project"}],"about":[{"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/types\/project"}],"author":[{"embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/users\/4"}],"replies":[{"embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/comments?post=49470"}],"version-history":[{"count":7,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project\/49470\/revisions"}],"predecessor-version":[{"id":49703,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project\/49470\/revisions\/49703"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/media\/49655"}],"wp:attachment":[{"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/media?parent=49470"}],"wp:term":[{"taxonomy":"project_category","embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project_category?post=49470"},{"taxonomy":"project_tag","embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project_tag?post=49470"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
ism\u00e9telt deporaliz\u00e1ci\u00f3ja hat\u00e1s\u00e1ra az NMDA-ioncsatorna megny\u00edl\u00e1sa a posztszinaptikus sejt hossz\u00fa t\u00e1v\u00fa potenci\u00e1ci\u00f3j\u00e1t (long term potentiation, LTP) okozza, de csak a megny\u00edl\u00e1s felt\u00e9teleinek egyidej\u0171 fenn\u00e1ll\u00e1sa eset\u00e9n. Ez\u00e9rt az NMDA-strukt\u00far\u00e1t koincidencia-receptornak is szokt\u00e1k nevezni. A szinaptikus plaszticit\u00e1s jelens\u00e9ge teszi lehet\u0151v\u00e9 k\u00e9t neuron k\u00f6z\u00f6tt a szinaptikus er\u0151ss\u00e9g megn\u00f6veked\u00e9s\u00e9t, ami a mem\u00f3ri\u00e1nak is az alapja.<\/p>\n
szerepet tulajdon\u00edtanak epilepszi\u00e1ban, demenci\u00e1ban, Parkinson-k\u00f3rban, alkohol-megvon\u00e1sban, agyi
trauma eset\u00e9n \u00e9s a cerebrovaszkul\u00e1ris betegs\u00e9gekben is. A folyamat l\u00e9nyege excessz\u00edv glutam\u00e1t felszabadul\u00e1sa, ami visszaford\u00edthatatlan k\u00e1lcium-be\u00e1raml\u00e1st, majd a neuron apopt\u00f3zis\u00e1t okozza. Az NMDA-alulm\u0171k\u00f6d\u00e9s pedig a szkizofr\u00e9nia egyik molekul\u00e1ris modellj\u00e9t jelenti. Az NMDA-receptor antagonist\u00e1i, a fenciklidin \u00e9s a ketamin hallucinog\u00e9n hat\u00e1s\u00fa molekul\u00e1k, melyek egyben kognit\u00edv diszfunkci\u00f3t is okoznak. A szkizofr\u00e9nia kandid\u00e1ns g\u00e9njei k\u00f6zu\u0308l t\u00f6bb (dysbindin, neuregulin 1, D-aminosav-oxid\u00e1z aktiv\u00e1tor) \u00e1ltal k\u00f3dolt, csak r\u00e9szben ismert funkci\u00f3j\u00fa feh\u00e9rje m\u0171k\u00f6d\u00e9se is az NMDA-neurotanszmisszi\u00f3 \u00fatvonal\u00e1ra konverg\u00e1l (Rethelyi \u00e9s mtsai, 2008, 2010). Kantrowicz \u00e9s Javitt (2010) emiatt a szkizofr\u00e9nia NMDA-hipot\u00e9zis\u00e9nek m\u00f3dos\u00edtott modellj\u00e9ben az NMDA-diszregul\u00e1ci\u00f3t a szkizofr\u00e9nia v\u00e9gs\u0151 k\u00f6z\u00f6s \u00fatj\u00e1nak nevezi, amelyre genetikai, molekul\u00e1ris \u00e9s k\u00f6rnyezeti hat\u00e1sok is \u201ebecsatlakozhatnak\u201d. V\u00e9gu\u0308l eml\u00edt\u00e9st \u00e9rdemel m\u00e9g egy n\u00e9h\u00e1ny \u00e9ve \u00fajonnan le\u00edrt, az NMDA-rendszer patol\u00f3gi\u00e1j\u00e1hoz k\u00f6thet\u0151 betegs\u00e9g. Az anti-NMDA-receptor encephalitis eset\u00e9n autoantitestek termel\u0151dnek az NMDA-receptorok ellen valamely keresztreakci\u00f3 r\u00e9v\u00e9n. Az akutan indul\u00f3 betegs\u00e9g v\u00e1ltozatos neurol\u00f3giai \u00e9s pszichi\u00e1triai tu\u0308netekkel j\u00e1rhat (Dalmau \u00e9s mtsai, 2008).<\/p>\n
today is nanomedicine, the utilization of nanotechnology in medicine. The long lists of innovative medicinal and other products, astonishing market and scientometric indicators
and the broad scale of promising therapeutic and diagnostic opportunities support the view
that nanomedicine heralds the future of medicine. The goals of this review are to provide
a comprehensive overview of the field, to compile the nanomedicines and other medical
products that are on the market, and to address in more detail the most successful trend,
targeted pharmacotherapy. Various nanocarriers (liposomes, micelles, polymer-conjugates,
polymerosomes, dendrimers, aptamers and carbon nanotubes) will be presented, along with
their targeting ligands, with special emphasis on liposomal doxorubicin (Doxil), the prototype of long-circulating, targeted chemotherapeutic nanomedicine. Nanotechnology holds
great promises for the field of neuropsychiatric pharmacotherapy as well, mainly through the
introduction of pharmaceutical agents passing the blood-brain barrier. The review presents
some of the approaches and examples of these attempts.<\/p>\n
Depression Scale for Schizophrenics (CDSS) in a Hungarian clinical population of patients with
schizophrenia. Method: One hundred patients diagnosed with schizophrenia according to
DSM-IV criteria were included in this study. Patients were all acutely admitted to the psychiatric unit of the Mer\u00e9nyi Hospital due to relapse. For evaluating convergent and discriminant
validity of the CDSS, scales measuring depression, negative symptoms, extrapyramidal side
effects, antipsychotic-induced dysphoria were assessed: Hamilton Depression Rating Scale
(HDRS), Positive and Negative Syndrome Scale (PANSS), Subject Well-being under Neuroleptic
Treatment (SWN), Drug Induced Extra-Pyramidal Symptoms Scale (DIEPSS), Clinical Global
Impressions-Severity (CGI-S), Clinical Global Impressions-Improvment (CGI-I). In order to
examine the test-retest reliability of the CDSS we conducted a 3 month-follow-up (n=83),
during which we applied the same set of scales. Results: The interrater reliability was high in
both the CDSS (ICC= 0.98) and the other scales (ICC= 0.75-0.98). Measures of internal consistency showed strong reliability, Cronbach alfa was 0.87, Guttman split-half reliabilty was 0.82.
Correlation calculations between CDSS and HAM-D resulted in high correlation: r=0.75-0.81.
CDSS showed lower correlations with PANSS-N, DIEPSS and SWN, indicating that this scale
is able to separate symptoms of depression from negative symptoms, extrapyramidal sideeffects and antipsychotic-induced dysphoria. Conclusion: The Hungarian version of CDSS
can be used to assess depression in schizophrenia and we recommend the introduction of
the scale into practice in Hungary.<\/p>\n
depression, schizophrenia<\/p>\n<\/div>\n