Triterpenoid-PEG Ribbons Targeting Selectivity in Pharmacological Effects.

(1) Background: To compare the effect of selected triterpenoids with their structurally resembling derivatives, designing of the molecular ribbons was targeted to develop compounds with selectivity in their pharmacological effects. (2) Methods: In the synthetic procedures, Huisgen 1,3-dipolar cycloaddition was applied as a key synthetic step for introducing a 1,2,3-triazole ring as a part of a junction unit in the molecular ribbons. (3) Results: The antimicrobial activity, antiviral activity, and cytotoxicity of the prepared compounds were studied.

WITHDRAWN: Autologous adipose tissue-derived stromal vascular fraction cells application in patients with osteoarthritis.

Ahead of Print article withdrawn by publisher

Microarray analysis of serum mRNA in patients with head and neck squamous cell carcinoma at whole-genome scale.

With the increasing demand for noninvasive approaches in monitoring head and neck cancer, circulating nucleic acids have been shown to be a promising tool. We focused on the global transcriptome of serum samples of head and neck squamous cell carcinoma (HNSCC) patients in comparison with healthy individuals. We compared gene expression patterns of 36 samples.

Functional alteration of cytochrome c oxidase by SURF1 mutations in Leigh syndrome.

Subacute necrotising encephalomyopathy (Leigh syndrome) due to cytochrome c oxidase (COX) deficiency is often caused by mutations in the SURF1 gene, encoding the Surf1 protein essential for COX assembly. We have investigated five patients with different SURF1 mutations resulting in the absence of Surf1 protein. All of them presented with severe and generalised COX defect.

[A new missense mutation of 574C>T in the SURF1 gene--biochemical and molecular genetic study in seven children with Leigh syndrome].

Background: Leigh disease, subacute necrotizing encephalopathy, is a serious mitochondrial disorder of energy-providing metabolism. Clinical presentation usually starts in infancy as a progressive neurodegenerative disorder with retardation and regression of psychomotor development. The most common form of the disease is associated with deficiency of the cytochrome c oxidase (COX) due to SURF1 gene mutations.

Activities of cytochrome c oxidase and citrate synthase in lymphocytes of obese and normal-weight subjects.

Background: Obesity represents a heterogeneous group of disorders associated with broad spectrum of metabolic and endocrine abnormalities. The metabolic changes in obesity may also concern the efficacy of mitochondrial system of energy provision. The aim of our study was to analyse activities of mitochondrial enzymes cytochrome c oxidase (COX) and citrate synthase (CS) in isolated lymphocytes of obese and normal-weight subjects.

[Disorders of mitochondrial energy metabolism in patients with the Kearns-Sayre syndrome].

Background: Kearns-Sayre syndrome is a multisystem disorder caused by rearrangements of mitochondrial genome including various deletions and/or duplications. The aim of the study is to analyse the impact of mitochondrial DNA (mtDNA) deletions on the mitochondrial energetic metabolism in five patients with Kearns-Sayre syndrome.

Methods And Results: The course of the disease is progressive in all patients.

Clonidine, but not ritanserin, suppresses kainic acid-induced automatisms in developing rats.

In young rats, systemic or local administration of kainic acid (KA) elicits scratching as the prevailing automatism whereas in adult rats, wet dog shakes (WDS) are usually recorded. We tested the effects of the alpha 2-adrenergic agonist clonidine (0.25 mg/kg, IP; also acting, however, on imidazoline receptors), which has been reported to block KA-induced WDS in adult rats and the 5-HT2 antagonist ritanserin (20 mg/kg, IP) in rats aged 7, 12, 18, 25, and 90 days treated IP with doses of KA that induce maximum number of automatisms with minimal early lethal effects (i.