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42. Abstrakta. CSIR 2012

Format:
braille, text, and regular print
Type:
model:article, article, Text, abstrakta, and TEXT
Subject:
radiologie intervenční--metody--trendy, ischemie mozku--terapie, cévní mozková příhoda--terapie, břišní dutina--patologie, diagnostické zobrazování--metody--trendy--využití, endoskopie--metody--trendy--využití, katetrizace--metody--využití, asistenti lékařů, zdravotní sestry, endovaskulární výkony--metody--trendy--využití, zaváděcí katetry--trendy--využití, stenty--využití, společnosti lékařské, and lidé
Language:
Czech
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

45. Activation of fat body in Periplaneta americana (Blattoptera: Blattidae) by hypertrehalosemic hormones (HTH): New insights into the mechanism of cell signalling

Creator:
Steele, John E.
Format:
print, text, and regular print
Type:
article, bibliography, model:article, and TEXT
Subject:
zoologie, entomologie, hmyz, Blattoptera, Blattidae, Periplaneta americana, hemolymfa, trehalosa, biosyntéza, kontrola biosyntézy, hypertrehalosemické hormony, mechanismus účinku, 595.2/.7, and 591.1
Language:
English
Description:
In cockroaches and certain other insects the concentration of trehalose in the hemolymph is increased by hypertrehalosemic hormone (HTH), a neuropeptide originating in the corpus cardiacum. A vital step in the action of HTH to promote conversion of glycogen stored in the fat body to trehalose is the activation of phosphorylase. The means by which HTH activates phosphorylase, with particular emphasis on its role in the regulation of intracellular calcium, is discussed. Additional information supporting the view that HTH stimulated synthesis of trehalose, and possibly its release from the trophocyte, is regulated by fatty acids and eicosanoids is presented., John E. Steele, and Lit
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

46. Acute appendicitis as a complication of varicella

Creator:
Pogorelić, Zenon, Biočić, Mihovil, Jurić, Ivo, Milunović, Klaudio Pjer, and Mrklić, Ivana
Format:
braille, text, and regular print
Type:
model:article, article, Text, kazuistiky, and TEXT
Subject:
lidé, dítě, mužské pohlaví, varicela--komplikace, akutní nemoc, klinický obraz nemoci, apendicitida--etiologie--patologie--virologie, apendektomie, výsledek terapie, histologie, apendix--patologie, and plané neštovice
Language:
English
Description:
Introduction: Obstruction of the appendiceal lumen is the primary cause of appendicitis. The most common causes of luminal obstruction are fecaliths and lymphoid follicle hyperplasia. Additionally, bacterial infections or enteric and systemic viral diseases can cause a reaction of the lymphoid follicle. Case presentation: An 11-year-old boy with active phase of chickenpox presented on our Pediatric surgery emergency department under the impression of acute appendicitis. An appendectomy was performed on the same day. An inflamed and edematous retrocecal appendix was removed during surgery. Histological investigation of the appendix revealed transmural acute inflammation, with diffuse proliferation of inflammatory cells, with characteristic intranuclear inclusion surrounded by a clear halo. The PCR analysis of peripheral blood and appendix tissue specimen revealed positive VZV DNA. Conclusion: We have shown that varicella-zoster virus infection of the appendix is associated with acute appendicitis and possibly also with severity of the disease., Zenon Pogorelić, Mihovil Biočić, Ivo Jurić, Klaudio Pjer Milunović, Ivana Mrklić, and Literatura 11
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

47. Acute Leukemias XV, Biology and Treatment Strategies

Creator:
Lemež, Petr
Format:
print, text, and regular print
Type:
model:article, article, Text, and TEXT
Subject:
kongresy jako téma, lidé, akutní lymfatická leukemie--farmakoterapie, akutní myeloidní leukemie--farmakoterapie, protokoly antitumorózní kombinované chemoterapie, reziduální nádor, imunoterapie--metody, receptory antigenů T-buněk--terapeutické užití, CTL019 buňky, and blinatumomab
Language:
Czech
Description:
Petr Lemež
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

48. Acyl-CoA Binding Domain Containing 3 (ACBD3) Protein in Huntington’s Disease Human Skin Fibroblasts

Creator:
Kratochvíľová, Helena, Rodinová, Marie, Sládková, Jana, Klempíř, Jiří, Lišková, Irena, Motlík, Jan, Zeman, Jiří, Hansíková, Hana, and Tesařová, Markéta
Format:
print, text, and regular print
Type:
model:article, article, Text, práce podpořená grantem, and TEXT
Subject:
lidé, dospělí, studie případů a kontrol, Huntingtonova nemoc--metabolismus, membránové proteiny--fyziologie--metabolismus, adaptorové proteiny signální transdukční--fyziologie--metabolismus, kůže--metabolismus--patologie, fibroblasty--metabolismus, buněčné linie--metabolismus, heterozygot, imunohistochemie, frakcionace buněk, lidské kožní fibroblasty, and Acyl-CoA binding domain containing 3 protein
Language:
Czech and English
Description:
Huntingtonova choroba (HD) je autozomálně dominantní neurodegenerativní onemocnění způsobené zvýšením počtu polyglutaminových repetic (> 35 repetic) v genu pro protein huntingtin. HD je charakteristická pomalými progresivními změnami pohybového aparátu a osobnosti, kdy tyto změny jsou často doprovázeny ztrátou tělesné hmotnosti. Do dnešního dne není znám přesný mechanizmus patofyziologie choroby. Poruchy pohybových funkcí reflektují masivní poškození specifických částí mozku (striatum), které bylo popsáno u pacientů s HD. V roce 2013 Sbodio et al [1] popsali zvýšené množství proteinu Acyl‑CoA binding domain containing 3 (ACBD3) ve striatu HD pacientů. Protein ACBD3 hraje nezastupitelnou roli v mnoha buněčných procesech, a to především díky interakci s různými vazebnými partnery. ACBD3 je esenciální při neuronálním dělení, neurodegeneraci, udržení lipidové homeostáze, stresové odpovědi, virové replikaci, apoptóze, udržení struktury golgiho komplexu. V této práci jsme prokázali nepřítomnost proteinu ACBD3 v mitochondriích v lidských kožních fibroblastech a navíc jsme potvrdili, že změny celkové hladiny proteinu ACBD3 ve fibroblastech HD pacientů nejsou konzistentní., Huntington’s disease (HD) is an autosomal‑dominant neurodegenerative disease caused by the expansion of polyglutamine repeats (> 35 repeats) in the nuclear gene for the huntingtin protein. HD is characterized by slow progressive changes in motor behaviour and personality that are sometimes accompanied by weight loss. To date, the exact mechanisms of HD pathophysiology have not been defined. Impaired motor behaviour reflecting massive and selective destruction of the striatum has been observed in patients with HD. Sbodio et al. [1] reported in 2013 that Acyl‑CoA binding domain containing 3 (ACBD3) protein levels were elevated in the striatum of HD patients and connected with higher neurotoxicity in HD. The ACBD3 protein plays essential roles in many different cellular functions via interactions with a multitude of partners. ACBD3 is involved in neuronal stem cell self‑renewal, neurodegeneration, lipid homeostasis, stress resistance, intracellular vesicle trafficking, organelle maintenance, viral replication and the apoptotic response. Herein, we found that ACBD3 in not present in the mitochondria in skin fibroblasts. Moreover, our findings also revealed that the total cellular level of ACBD3 is not consistent among the fibroblasts of HD patients., and H. Kratochvíľová, M. Rodinova, J. Sladkova, J. Klempir, I. Liskova, J. Motlik, J. Zeman, H. Hansíková, M. Tesarova
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

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