Psoriasis is a disease with a genetic background (4). Several psoriasis susceptibility loci (PSORS) have been found on various chromosomes: PSORS1 on 6p21.3, PSORS2 on 17q, PSORS3 on 4q, PSORS4 on 1q21, PSORS5 on 3q21, PSORS6 on 19p, PSORS7 on 1p, PSORS8 on 16q, PSORS9 on 4q31, PSORS10 on 18p11, PSORS11 on 5q31-q33 and PSORS12 on 20q13. (27). However, the exact genes and their functions, or their respective malfunctions, in psoriasis and arthritis have not been unambiguously identified. Recently, it has been argued that PSORS1 may indeed be the HLA-Cw*06 allele encoding the HLA-Cw6 molecule (35).
Psoriasis is a chronic inflammatory disease of skin that also often affects joints and nails. This disorder is characterized by hyperproliferation of keratinocytes, activation of angiogenesis, vasodilatation and mainly by lymphocyte infiltration of dermis and epidermis (45). The process of maturation of keratinocytes is accelerated and thus not quite terminated. Psoriatic lesion appears on skin.
Skin manifestations are typically red bounded areas of different size and shape with characteristic silvery scales (9). Lesions appear mostly on the skin of elbows and knees, scalp including genitals. Individual manifestations differ in size and severity from localized lesions to whole body involvement. Very often psoriasis affects nails of hands and feet. It can also cause inflammatory changes on joints, named as psoriatic arthritis. Similarly to rheumatoid arthritis and sclerosis multiplex, psoriasis is classified as an immune mediated inflammatory disorder. Those disorders are characterized by chronic progression of an inflammatory process and important role of TNF alpha. Because of the role of TNF alpha in pathogenesis, we can use its inhibitors in therapy. It also affects progress of different comorbidities such as diabetes mellitus 2 and cardiovascular problems (21). Patients with psoriasis have often other risk factors for atherosclerosis such as lipid metabolism disorders and overweight (37).
Synthesis and enantioseparation of derivatives of propranolol
Propranolol is one of the first prepared and in therapeutic praxis used beta- adrenolytics. In this paper novel derivatives of propranolol with cyclohexylamino and pyrrolidin-1-yl groups in hydrophilic part were prepared. HPLC-enantioseparation propranolol (as reference compound) and of the prepared derivatives has been achieved using a Chiralpak AD CSP based on the amylose tris (3,5-dimethylphenylcarbamate).(R)-enantiomer of the propranolol was prepared by stereoselective synthesis using Jacobsen catalyst.
Within the framework of the study of the synthesis and high-performance liquid chromatography (HPLC) enantioseparation the series of 9 derivatives of 3-hydroxyphenylethanone was prepared by a well-tried method. The structure of the prepared compounds was confirmed on the basis of interpretation of the IR, UV, 1H NMR and 13C NMR spectra. An enantioseparation of prepared compounds was performed using HPLC on a native teicoplanin (Chirobiotic T) and the amylose tris (3,5-dimethylphenylcarbamate) (Chiralpak AD) chiral stationary phases, which is more suitable for the enantioseparation of all prepared compounds especially with heterocycles in the basic part of a molecule.
This article describes a preparation of some new compounds of the aryloxyaminopropanol type derived from 4-hydroxyphenylpropan- 1-one with phenylamino, cyclohexylamino and isobutylamino group in the hydrophilic part and methoxymethyl or ethoxymethyl substituent in the lipophilic part of the molecule. The purity of the prepared compounds was checked by thinlayer chromatography and the structure was confirmed on the basis of interpretation of the IR, UV, 1H NMR and 13C NMR spectra. An enantioseparation of the prepared compounds was performed by using high-performance liquid chromatography on an amylase tris(3,5-dimethylphenylcarbamate) (Chiralpak AD) and native teicoplanin (Chirobiotic T). The chromatographic results such as retention, separation and resolution factors have shown that Chiralpak AD is more suitable for enantioseparation of some of the prepared compounds.
This review article is concentrating on the news in the pathophysiology of chronic venous insufficiency (CVD). Despite ongoing progress in understanding the molecular aspects of CVD the exact mechanism of its development remains unclear. Many different factors may play role in the pathogenesis of CVD, including changes in hydrostatic pressure, valvular incompetence, increased capillary permeability, endothelial dysfunction, activation of leukocytes, deep venous obstruction, capillary microthrombosis, ineffective function of calf muscle pump, biochemical and structural changes in the vessel wall, extracellular matrix alteration, and several other mechanisms. A better understanding of the pathophysiology is an important step in the finding of new potential treatment.
The aim of our study was to determine the prevalence of toxocariasis in Bratislava and smaller towns in western Slovakia. During 2006–2011, sand samples collected from 121 sandpits were investigated: 63 sandpits were from Bratislava City and 58 from sandpits in towns outside Bratislava (Malacky, Pezinok Stupava). In Bratislava, 27% of examined sandpits were contaminated with Toxocara spp. eggs. In smaller towns eggs of Toxocara spp. were found from three sandpits (6.8 %) of Pezinok and Stupava only. In Malacky, no faeces and no eggs were found in any sandpits. Faecal samples of 1436 dogs and 263 cats were investigated. T. canis eggs were found in the faeces of 16.5 % dogs and T. cati in 18.6 % of examined cats. Toxocariasis of dogs was significantly higher in smaller towns such as the city Bratislava (χ2 = 10.88 for P ≤ 0.001). The difference in prevalence of T. cati in cats bred in Bratislava and outside Bratislava was not confirmed (P ≤ 0.05). 382 pregnant women were examined by ELISA. Anti-Toxocara antibodies were detected in 32 women (8.4 %). The difference in seroprevalence of women coming from Bratislava (6.6 %) and smaller towns outside Bratislava (11.0 %) was not statistically significant (χ2 = 1.6; P ≤ 0.05).