Magyarország Zenetörténete sorozat: 18. és 20. századi kötetek = Hungarian Music history: 3. and 5. vol.

A pályázat a Magyarország Zenetörténete III. kötetének kutatómunkáját segítette a) kötetfejezetek ill. első fogalmazványok b) a témához kapcsolódó publikációk c) a kötetfejezetek hátterét biztosító adatbázisok ill. 18. századi művek partitúráinak létrehozása által. a) Kötetfejezetek készültek a katolikus templomok zenei életéről, a zenészek foglalkoztatásának társadalmi körülményeiről, jövedelemviszonyairól a 18. századi Magyarországon b) Farkas Z., Sas Á. és Szacsvai K. tanulmányokat publikáltak és nemzetközi konferencián előadásokat tartottak. c) hat 18. ill. kora 19. századi kompozíció (Werner, Zimmermann, Novotni, Lickl, Zmeskall) partitúrája készült el (összesen ca. 610 partitúraoldalnyi számítógépes kottagrafika). A 20. századi kutatások eredményei a zeneműkiadás- és koncerttörténeti alapkutatások, tíz-illetve húszezres nagyságrendű adatbázisaiban (1.,3.) és a zeneszerzői életműkutatások összefoglaló publikációiban (1-7 kismonográfia, magyar és angol nyelven a Magyar zeneszerzők sorozatban,) jelentkeztek. 1. Lezárult a több éves kutatás: A magyar zeneműkiadás története a két világháború között témakörben. 2. A zeneszerzői életművek feldolgozása 10 szerzői alapkutatással gyarapodott. Eredményként 7 kismonográfia jelent meg. 3. A befejezés stádiumába jutott a Budapesti Hangversenyek Adattára (1900-1945) adatbázisa, 15.000 koncertet rögzít: a szerzők, a zeneművek, az előadók és a helyszínek szerint. | One of the principal aims of the project was to promote research for the production of the 3rd volume of the series History of Music in Hungary (1686-1820) a) producing chapters and drafts b) publishing articles and papers c) producing databases and scores which can form a basis for the analitical chapters. a) Chapters have been finished on Music Life of Roman Catholic Churches in 18th Century Hungary b) Z. Farkas, A. Sas, K. Szacsvai have published articles and read papers in international conferences c) Scores of 5 compositions by Werner, Zimmermann, Novotni, Lickl, Zmeskall were compiled from original manuscripts. The results of research into 20th-century music, basic research into music publishing and the history of concerts have appeared in ten to twenty thousand-character-long databases (1, 3) and in comprehensive publications about the composers' lifework (7 monographs in the series Magyar zeneszerzők) 1. The research project entitled The history of Hungarian music publishing between the two world wars and lasting several years has been concluded. 2. To the elaboration of the composers' oeuvres ten basic research results have been added and seven short monographs have been published. 3. The database of the List of Budapest Concerts (1900-1945) has reached the stage of conclusion, recording about 15,000 concerts according to composers, works, performers, and sites

Neuroprotective effects of repeated transient global ischemia and of kynurenine adminsitration induced by four-vessel occlusions on hippocampal CA1 neurons.

The hippocampal CA1 subfield is a brain region that is particularly sensitive to hypoxia. Although this subfield is selectively vulnerable to ischemic injuries manifested in delayed neuronal death (DND), the mechanism leading to neuronal degeneration is not fully understood. Burda recently reported that a second pathophysiological stress, applied within a suitable time, offers an opportunity for salvaging neurons in the CA1 region against DND (Neurochem. Res., 30: 1397-1405, 2005). In our study, NeuN immunohistochemistry was applied to detect survival CA1 neurons, while Fluoro-Jade B staining was used to evaluate the number of injured neurons after interventions resulting in transient global ischemia. Four groups of animals were used: 1: intact controls; 2: sham controls (2 vertebral arteries coagulated (2VAC), but 2 carotids sham-operated); 3: 2VAC + 2 carotids occluded (2CA) for 10 min; 4: 2VAC + 2CA (10 min) + 2 days later, a repeated 2CA (5 min). In group 3 (2VAC + 2CA (10 min)), marked cell destruction was found in the CA1 subfield: only 36.4% of the CA1 neurons survived. However, in group 4 (5-min second ischemic insult), the proportion of surviving cells in the CA1 region was 59.3%. There was no significant difference in CA1 cell loss between groups 1 and 2. Our findings suggest that the second ischemic stress, 2 days after the first ischemia induced by 2VAC + 2CA can be efficient in the prevention of DND. Neuroprotective effect was also found in four-vessel occlusion models after kynurenine (i.v.) administration

Increased frequency of temporal acoustic window failure in rheumatoid arthritis: a manifestation of altered bone metabolism?

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Assessment of cognitive function in female rheumatoid arthritis patients: associations with cerebrovascular pathology, depression and anxiety

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Tetraplegia sikeres multidiszciplináris kezelése mellkassebészeti műtéttel. Unicentrikus mediastinalis Castleman-betegség esete = Successful multidisciplinary management of tetraplegia with a thoracic operation Unicentric, mediastinal Castleman disease

Absztrakt: A Castleman-betegség egy ritka, lymphoproliferativ betegség, melynek pontos oka ismeretlen. Diagnosztikájának alapja az adekvát szövettani vizsgálat. Míg az unilocularis formánál a betegség a leggyakrabban a mellkast érinti, és az épben történő sebészi eltávolítás a tünetek megszűnését eredményezheti, addig a multilocularis formánál egyéb kezelési formák egészíthetik ki vagy válthatják fel a műtéti eltávolítást. Munkánkban egy Castleman-betegség miatt multidiszciplináris kezelésen átesett beteg esetét mutatjuk be. Az 56 éves férfi betegnél kivizsgálása előtt 18 héttel, egy felső légúti infekciót követően beszédnehezítettség, nyelészavar, felső és alsó végtagi progresszív paresis jelentkezett. Plazmaferézisre a beteg panaszai átmenetileg megszűntek ugyan, de a sebészi mintavételek a mellkas-CT-n látott mediastinalis lymphadenomegalia eredetét nem tudták igazolni. Így az 5 cm-es subcarinalis nyirokcsomó eltávolítása vagy mintavételezése miatt került a beteg osztályunkra. Átvételkor mind a négy végtagon jelentős atrófia, hipotónia, tetraplegia volt látható, és testszerte areflexia igazolódott. Osztályunkon posterolateralis thoracotomiából eltávolítottuk az 5,5 × 3,5 cm-es subcarinalis nyirokcsomó-konglomerátumot. A szövettani vizsgálat Castleman-betegséget jelzett. 3 nappal a műtét után a végtagok mozgása megindult, a 9. napon már járókerettel járóképessé vált, ezt követően neurológiai rehabilitációs osztályra került. Ekkor a felső végtagokban közel megtartott, míg az alsó végtagokban 4/5-ös izomerőt észleltek. Ezt követően a beteg metilprednizolon-, B1-vitamin-, kalcium-citrát- és famotidinkezelésben részesült; 2 héttel átvétele után otthonába bocsátották, ekkor már járókeret nélkül biztonságosan közlekedett. Tünetei 3 hónappal a műtét után csaknem teljes mértékben megszűntek. A Castleman-betegség diagnosztikája és kezelése multidiszciplináris feladat. Ha a páciens műtéti teherbíró képessége engedi, akkor az unilocularis Castleman-betegség terápiás eszköztárában a sebészeti eltávolításnak kiemelt szerepe kell, hogy legyen. OrvHetil. 2020; 161(1): 33–38. | Abstract: Castleman disease is a rare lymphoproliferative disease the exact cause of which is not known. The diagnosis is based on the adequate histological examination. While in the unifocal form, the disease most commonly affects the chest, and symptoms may resolve as a result of intact excision of the tumour; other treatment methods may be performed in addition to or instead of surgical incision in the case of the multifocal form. We present the case of a patient with Castleman disease who received multidisciplinary treatment. Speech difficulty, dysphagia, and progressive paresis occurred in the upper and lower extremities of the 56-year-old male patient 18 weeks before his check-up examinations. Although the complaints temporarily resolved with plasmapheresis, surgical sampling could not confirm the origin of the mediastinal lymphadenomegaly detected with thoracic CT. The patient was admitted to our department to remove the 5 cm large subcarinal lymph node or to gain a tissue sample from it. On admission, significant atrophy, hypotonia and tetraplegia were seen in the four extremities, and areflexia was detected all over the body. The 5.5 × 3.5 cm large subcarinal lymph node conglomerate was removed from posterolateral thoracotomy. Histology was performed, Castleman disease was confirmed. 3 days after the surgery, the patient was able to move the extremities, and then on the 9th postoperative day, the patient could walk using a walking frame, and he was transferred back to the Department of Neurorehabilitation. At transfer, the muscle strength of the upper extremities was almost intact, and 4/5 muscle strength was detected in the lower extremities. After this, methylprednisolone, vitamin B1, calcium citrate, famotidine therapy was administered, and 2 weeks after his transfer, he was discharged home; at that time, the patient was able to walk safely without a walking frame. The symptoms resolved almost completely 3 months after the surgery. Diagnosis and treatment of Castleman disease are multidisciplinary tasks. If the patient is suitable for surgery, surgical removal has to play a key role in the treatment of unifocal Castleman disease. Orv Hetil. 2020; 161(1): 33–38

Mitochondria, oxidative stress and the kynurenine system, with a focus on ageing and neuroprotection

In this review, the potential causes of ageing are discussed. We seek to gain insight into the main physiological functions of mitochondria and discuss alterations in their function and the genome, which are supposed to be the central mechanisms in senescence. We conclude by presenting the potential modulating role of the kynurenine pathway in the ageing processes. Mitochondrial dynamics are supposed to have important physiological roles in maintaining cell homeostasis. During ageing, a decrease in mitochondrial dynamics was reported, potentially compromising the function of mitochondria. Mitochondrial biogenesis not only encompasses mitochondrial dynamics, but also the regulation of transcription and translation of genes, and mitochondria are supposed to play a prominent role in cell death during senescence. Defects in the mtDNA replication machinery and failure in the repair of mtDNA might result in the accumulation of mutations, leading to mitochondrial dysfunction and bioenergetic failure of the cell. The role of reactive oxygen species (ROS) in the ageing processes is widely acknowledged. Exaggerated oxidative damage to mDNA is supposed to take place during senescence, including single-nucleotide base alterations, nucleotide base pair alterations, chain breaks and cross linkage. A broad repertoire for the repair of DNA faults has evolved, but they do not function efficiently during senescence. Poly (ADP-ribose) polymerase (PARP) is an enzyme that assists in DNA repair, i.e., it participates in the repair of single-stranded DNA nicks, initiating base excision repair (BER). In the case of extensive DNA damage, PARP-1 becomes overactivated and rapidly depletes the intracellular NAD+ and ATP pools. This results in a profound energy loss of the cell and leads to cell dysfunction, or even cell death. Alterations in the kynurenine system have been linked with ageing processes and several age-related disorders. The kynurenine pathway degrades tryptophan (TRP) to several metabolites, among others kynurenine (KYN), kynurenic acid (KYNA) and quinolinic acid (QUIN). The end product of the route is NAD+. The first metabolic reaction is mediated by TRP-2,3-dioxygenase (TDO) or indolamine-2,3-dioxygenases (IDO), the latter being induced by inflammation, and it is thought to have a significant role in several disorders and in ageing. Research is currently focusing on the KYN pathway, since several intermediates possess neuro- and immunoactive properties, and hence are capable of modulating the activity of certain brain cells and inflammatory responses. During ageing, and in many age-associated disorders like obesity, dyslipidaemia, hypertension, insulin resistance and neurodegenerative diseases, low-grade, sustained inflammation and upregulation of IDO have been reported. However, TRP downstream catabolites create a negative feedback loop by weakening the activated immune system through several actions, including a decline in the Th1 response and an enhancement of Th2-type processes. The broad actions of the KYN-intermediates in brain excitation/inhibition and their role in regulating immune responses may provide the possibility of modifying the pathological processes in an array of age-associated diseases in the future. © 2018 by the authors