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Conjugate anti-endotoxin vaccines

100%

Lugowski C., Jachymek W., Niedziela T.

Bulletin of the Veterinary Institute in Puławy

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1998

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tom 42

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nr 1

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Inhibition of serum amyloid A protein amyloid formation

84%

Sosnowska M., Jankowska E.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

The acute-phase protein serum amyloid A (SAA) is present in the bloodstream at the concentration below 1 µM under physiological conditions, but its level increases significantly during the acute-phase response following infection or inflammatory condition. A consequence of the long-term elevated SAA concentration is deposition of normally soluble serum amyloid A in the form of insoluble fibrils, impairing tissue structure and function. These deposits cause development of a secondary type amyloidosis, called amyloid A protein (AA) amyloidosis, which results in a death of thousands of people per annum around the world. The ability of SAA to form amyloids seems to be connected with the N-terminal portion of the molecule. The capacity of the synthetic peptides derived from the N-terminal sequence of human or mice SAA to form fibrils in vitro proves that the most amyloidogenic region is embedded within the protein’s first 15 amino acids. We decided therefore to use peptides consisting of 11–15 amino acids and the sequence derived from the N-terminus of the parent aggregating protein as a research tool for investigation of the molecular recognition and self-assembly mechanisms that promote the formation of SAA amyloid fibrils deposits. In this study, we tested the hypothesis that non-aggregating very short peptides derived from SAA sequence would interact with the analogous region in the protein molecule or its aggregation-prone N-terminal fragment, and block its assembly into oligomers and amyloid fibrils. We designed and synthesized a peptide with the sequence 1RSFFS5, derived from the human SAA primary structure, and then tested it as a potential inhibitor of the aggregation process of SAA protein. The hypothesis about the role of aromatic interactions in amyloid fibril formation led us to test another peptide: 17LVFF20, which is derived from the sequence of Aβ. We tested propensity of the N-terminal segment (1–15) of mice SAA for amyloid fibrils formation, incubating it either alone or together with the potential inhibitors. Thioflavin T (ThT) fluorescence test was used to detect amyloid fibrils formation. These tests confirmed that the designed peptides are able to diminish propensity of the aggregation-prone SAA peptides to form amyloid fibrils. There are currently no effective medical treatment of diseases associated with the systemic amyloidosis. We believe that results of the presented project open up new possibilities in designing compounds that are able to prevent formation of amyloid deposits and could be a starting point for the design of peptidomimetic molecules more suitable as potential drugs. The work was supported by grant NCN nr 2011/03/N/NZ5/01460 and grant BMN No 538-8440-1042-12.

3

Sphingomyelin-cholesterol liposomes. Effect of natural resorcinolic amphiphiles on their properties

84%

Przeworska E., Kamps J. A. A. M., Scherphof G. L., Kozubek A.

Cellular and Molecular Biology Letters

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1999

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tom 04

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nr 2

4

Plasminogen activator inhibitor 1 [PAI-1] 1334G-A genetic polymorphism in colorectal cancer

67%

Smolarz B., Romanowicz-Makowska H., Kulig A.

Acta Biochimica Polonica

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2003

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tom 50

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nr 2

Plasminogen activator inhibitor 1 (PAI-1) content in colorectal cancer tissue extracts may be of strong prognostic value: high levels of PAI-1 in tumours predict poor prognosis. The gene encoding PAI-1 is highly polymorphic and PAI-1 gene variability could contribute to the level of PAI-1 biosynthesis. In the present work the distribution of genotypes and frequency of alleles of the 1334G/A polymorphism in 92 subjects with colorectal cancer in samples of cancer tissue and distant mucosa samples as well as in blood were investigated. Blood samples age matched healthy individuals (n = 110) served as control. The 1334G/A polymorphism was determined by PCR amplification using allele specific primers. No differences in the genotype distributions and allele frequencies between blood, distant mucosa samples and cancer tissue were detected. However, the distribution of the genotypes of the 1334G/A polymorphism in patients differed significantly (P < 0.05) from those predicted by the Hardy-Weinberg equilibrium. There were significant differences in the frequencies of alleles between the colorectal cancer subjects and controls (P < 0.05). The results support the hypothesis that the 1334G/A polymorphism may be associated with the incidence of colorectal cancer.

5

Mechanisms of acute respiratory distress syndrome: role of surfactant changes and mechanical ventilation

67%

Verbrugge S. J. C., Sorm V., Lachmann B.

Journal of Physiology and Pharmacology

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1997

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tom 48

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nr 4

6

Signal transduction pathway leading to prevention of atherosclerosis: role of witamin E

67%

Nalecz M. J.

Biophysics of Membrane Transport

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1994

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tom 12

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nr 1

7

TEM studies on morphological 'junctions' between Trichinella spiralis larvae and mouse skeletal muscle cells with particular emphasis on the early changes in host muscles

67%

Dabrowska J., Walski M., Machnicka B., Grytner-Ziecina B.

Acta Parasitologica

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2008

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tom 53

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nr 4

Larvae of the parasitic nematode Trichinella spiralis migrate via the bloodstream or the lymphatic system to the skeletal muscle cells where they induce multiple alterations in the intracellular environment leading to the formation of nurse cells. The “nurse cell-T. spiralis larva” complex is composed of a transformed fragment of a skeletal muscle cell and the wall of the larva. The pathological process responsible for the formation of this complex, known as basophilic transformation, is essential for the development of T. spiralis larvae, but it still not known how newborn larvae penetrate the transformed fragment of the muscle cell. In this study, we aimed to characterize the ultrastructure of the region of the nurse cell in direct contact with the larval wall, after one and two weeks of T. spiralis infection in mice. For this purpose, a transmission electron microscope fitted with a goniometer was used to make observations of samples tilted at an angle of ±40° relative to the axis of the electron beam. Examination of electron micrographs revealed the continuity of the nurse cell membrane adjacent to the larval surface and the presence of a large quantity of glycogen particles close to the inner surface of this membrane. Our results showed that death of the T. spiralis larvae was associated with destruction of the contact region between the larval wall and the adjacent surface of the nurse cell. We conclude that the T. spiralis larva does not penetrate the nurse cell, but a morphological “junction” is formed between the larval wall and the cell membrane.

Ograniczanie wyników

Conjugate anti-endotoxin vaccines

Inhibition of serum amyloid A protein amyloid formation

Sphingomyelin-cholesterol liposomes. Effect of natural resorcinolic amphiphiles on their properties

Plasminogen activator inhibitor 1 [PAI-1] 1334G-A genetic polymorphism in colorectal cancer

Mechanisms of acute respiratory distress syndrome: role of surfactant changes and mechanical ventilation

Signal transduction pathway leading to prevention of atherosclerosis: role of witamin E

TEM studies on morphological 'junctions' between Trichinella spiralis larvae and mouse skeletal muscle cells with particular emphasis on the early changes in host muscles