Short-winged (brachypterous) and long-winged (macropterous) adult females of Pyrrhocoris apterus (L.) originating from a Mediterranean population (Israel) were analyzed for their adipokinetic responses. The adipokinetic response, expressed as an increase of haemolymph lipids after injection of adipokinetic hormone from Locusta migratoria (Lom-AKH-I), was assessed in relation to age and dose of the hormone. We demonstrate in this study that the adipokinetic responses induced by bug's corpora cardiaca extract and Lom-AKH-I were dose-dependent for both brachypterous and macropterous females. Significant differences between the morphs were recorded for doses >= 0.25 corpora cardiaca equivalent (P < 0.01) and doses >= 0.25 pmol Lom-AKH-I (P < 0.05). The haemolymph lipid elevations induced in both morphs by 2 pmols Lom-AKH-I are comparable with that induced by crude extract of one pair of the bug's own corpora cardiaca. The age-dependent test showed much higher adipokinetic responses (P < 0.01) in macropterous females (>= 5 days old) than in the brachypterous females of the same age, when treated with 2 pmols Lom-AKH-I. Starting from day 7, the concentration of haemolymph lipids was also considerably higher (2.5-5 times) in macropterous females than in the brachypterous ones. The obtained data indicate that difference in mobilization of lipids between brachypterous and macropterous females is a geographically independent feature and represents a true wing morph characteristic of P. apterus., Dalibor Kodrík, Radomír Socha, and Lit
BACKGROUND: Radio frequency (RF) and chemical peels have been used for nonablative skin rejuvenation. Both of these cause collagen remodeling in the dermis and neo-collagen formation resulting in facial rejuvenation. There is limited literature on the evaluation of collagen remodeling by objective methods. OBJECTIVE: To compare the benefits of monopolar radiofrequency and glycolic acid peels in facial rejuvenation with regards to histopathology and Ultrabiomicroscopic sonography (UBM). METHODOLOGY: In this study, forty patients with mild to moderate photoaging received four treatments with 3 weeks interval of monopolar radiofrequency on one side of face and glycolic acid peels in increasing concentrations (NeostrataR) on the other side. Pre and post treatment, 2 mm biopsies were taken from both preauricular areas and Ultrasonography using a 35 MHz probe was done from outer canthus of eye and nasolabial folds from both sides of face. A blinded assessment was done to measure the increase in the grenz zone and dermal thickness. RESULTS: In 35/40 patients there was a significant increase in the grenz zone on histopathology and decrease in subepidermal low-echogenic band (SLEB) on UBM of the nasolabial folds on both sides of the face (p < 0.05). CONCLUSION: Radiofrequency and chemical peels showed equal efficacy in the treatment of facial rejuvenation. and D. V. Wakade, C. S. Nayak, K. D. Bhatt
Hereditární hemoragická teleangiektázie neboli morbus Rendu‑Osler‑Weber je fibrovaskulární dysplazie s autozomálně dominantní dědičností charakteristická přítomností teleangiektázií a arteriovenózních malformací kůže, sliznic a vnitřních orgánů. Plicní arteriovenózní malformace jako zdroj septických embolů mohou zapříčinit vznik mozkového abscesu, který tak bývá prvním a často jediným projevem heriditární hemoragické teleangiektázie. V práci jsou prezentovány tři kazuistiky pacientů trpících touto chorobou, kde prvním a závažným příznakem byl vzniklý mozkový absces. Protože se jedná o relativně vzácné onemocnění, nebývá vždy zvažováno v rámci diferenciální diagnostiky a tím pádem ani diagnostikováno. U každého pacienta s mozkovým abscesem je nezbytné na toto onemocnění pomýšlet a v případě podezření je nutné jej řádně vyšetřit. Při verifikované plicní arteriovenózní malformaci je třeba ji ošetřit a zabránit tak vzniku recidivujících mozkových abscesů. Péče o tyto pacienty je komplexní a multioborová., Hereditary hemorrhagic telangiectasia or Rendu‑Osler‑Weber disease is an autosomal‑dominant disorder that results in fibrovascular dysplasia and is characterized by telangiectases and arteriovenous malformation of the skin, mucosa and viscera. Pulmonary arteriovenous malformations as a source of septic emboli may give rise to brain abscess that so often is the first and only clinical manifestation of hereditary hemorrhagic telangiectasia. Three cases of patients suffering from this disease with brain abscess as the first and serious symptom are presented. Since this is a relatively rare disease, it is not always considered in the differential diagnosis and thus not diagnosed. This disease has to be considered in patients with brain abscess and, in case of a suspicion, it must be properly examined. When pulmonary arteriovenous malformation is verified, it has to be treated in order to prevent recurrent brain abscesses. Care of these patients should be comprehensive and multidisciplinary. Key words: hereditary hemorrhagic telangiectasia – Rendu-Osler-Weber disease – brain abscess – arteriovenous malformation – epistaxis – endoglin The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study. The Editorial Board declares that the manuscript met the ICMJE “uniform requirements” for biomedical papers., and G. Hanoun, V. Vybíhal, M. Sova, J. Boudný, T. Svoboda, M. Smrčka
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
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