Wyniki wyszukiwania

1

Discovery, mechanism and expected clinical significance of selective cytotoxicity of 2-chloro-2'-deoxyadenosine [2-CdA]

100%

Grieb P.

Archivum Immunologiae et Therapiae Experimentalis

|

1994

|

tom 42

|

nr 1

2

Wladyslaw Polinski and the discovery of the endemic, relict fauna of the Ohrid Lake

84%

Riedel A.

Folia Malacologica

|

1998

|

tom 06

|

nr 1-4

3

From wheat to Arabidopsis: discovery and analysis of novel egg cell specific genes

84%

Sprunck S., Bellmann B., Gebert M., Baumann U., Dresselhaus T.

Acta Biologica Cracoviensia. Series Botanica. Supplement

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2005

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tom 47

|

nr 1

4

100th anniversary of the discovery of the human adrenal fetal zone by Stella Starkel and Leslaw Wegrzynowski: how far have we come?

67%

Malendowicz L.

Folia Histochemica et Cytobiologica

|

2010

|

tom 48

|

nr 4

5

Gastric cancer and Helicobacter pylori infection

67%

Konturek P. C., Konturek S. J., Brzozowski T.

Journal of Physiology and Pharmacology. Supplement

|

2006

|

tom 57

|

nr 3

51-65

The Nobel prize in Physiology and Medicine in 2005 was presented to Barry Marshall and Robin Warren for their discovery of Helicobacter pylori (Hp), but only the involvement of this germ in gastritis and peptic ulcer has been mentioned in the award sentence, while numerous epidemiological, clinical and experimental studies and reports emphasized the crucial role of Hp in pathogenesis of gastric cancer (GC). This review is based on the old concept proposed by P. Correa much before the discovery of spiral bacteria in the stomach, postulating the cascade of mucosal changes from acute/chronic gastritis into the atrophic gastritis with intestinal metaplasia and finally to dysplasia and GC. It is now widely accepted view that Hp infection is the major initiator of the inflammatory and atrophic changes in gastric mucosa accompanied by an over-expression of certain growth factors such as gastrin as well as of cyclooxygenase-2 (COX-2) and anti-apoptotic proteins including survivin and B-cl2, leading to proliferation of mutated atrophic cells, excessive angiogenesis, inhibition of apoptosis and formation of gastric tumour. All the morphological and biochemical changes associated with the transformation of mucosal cells into the cancer cells can be traced in excellent experimental model of gastric cancerogenesis induced by infection of Hp in Mongolian gerbils. Since the eradication therapy was proved in several prospective clinical trials to greatly reduce the incidence of GC and this was confirmed on the gerbil model of Hp-induced GC, it has been postulated; a) that Hp is the major causal factor in pathogenesis of GC and b) that the only rational approach in attempt to reduce the occurrence of GC is the global eradication of Hp.

6

Serum response factor: discovery, biochemistry, biological roles and implications for tissue injury healing

59%

Chai J., Tarnawski A. S.

Journal of Physiology and Pharmacology

|

2002

|

tom 53

|

nr 2

Serum response factor (SRF) is a transcription factor, which binds to a serum response element (SRE) associated with a variety of genes including immediate early genes such as c-fos, fosB, junB, egr-1 and –2, neuronal genes such as nurr1 and nur77 and muscle genes such as actins and myosins. By regulating expression of these genes, SRF controls cell growth and differentiation, neuronal transmission as well as muscle development and function. SRF can be activated by a variety of agents, including serum, lysophosphatidic acid (LPA), lipopolysaccharide (LPS), 12-O-tetradecanoylphorbol- 13-acetate (TPA), cytokines, tumor necrosis factor-. (TNF.... ), agents that increase intracellular Ca 2+, T-cell virus1 activator protein, hepatitis B virus activator proteins pX, activated oncogenes and protooncogenes as well as extracellular stimuli such as antioxidant and UV light. SRF itself is regulated by both cellular signal transduction pathways and interaction with other transcription factors e.g. Sp1, ATF6 and myogenic regulatory factors. Its biological function is best eluci-dated for myocardium. Specific cardiac SRF transgenesis demonstrated that overex-pression of SRF caused hypertrophic cardiomyopathy in mouse and the mouse died of heart failure within 6 months after birth. Other transgenic data suggested that suf-ficient SRF was needed for embryogenesis and early development. Since SRF is important regulator of numerous genes involved in cell growth and differentiation, including muscle and neural components, SRF may also play a crucial role in tissue injury and ulcer healing, e.g. healing of gastrointestinal ulcers.

Ograniczanie wyników

1 Acta Biologica Cracoviensia. Series Botanica. Supplement

1 Archivum Immunologiae et Therapiae Experimentalis

1 Folia Histochemica et Cytobiologica

1 Folia Malacologica

1 Journal of Physiology and Pharmacology

1 Journal of Physiology and Pharmacology. Supplement

1 Baumann U.

1 Bellmann B.

1 Brzozowski T.

1 Chai J.

1 Dresselhaus T.

1 Gebert M.

1 Grieb P.

1 Konturek P. C.

1 Konturek S. J.

1 Malendowicz L.

1 Riedel A.

1 Sprunck S.

1 Tarnawski A. S.

1 2010

1 2006

1 2005

1 2002