[Influence of antiplatelet drugs (AD) on the efectiveness of combined therapy of small cell lung cancer. Part II. Influence of treatment on time of remission and patients survival].

In the experimental work evidence has been shown concerning the important relationship that exsists between the neoplastic process and blood coagulation status. In the 1st part of the paper it was shown that antiplatelet drugs (AD) prolonged bleeding and clotting time, increased the threshold ADP and collagen concentration causing platelets aggregation, as well as increased platelet aggregation ratio. The used AD (Defibrotide, Ticlide) resulted in activation of the plasma fibrynollytic system as expressed by the shortenning of ECLT, lowering of fibrinogen level and increasing FDP.

[Influence of antiplatelet drugs (AD) on the efectiveness of combined therapy in patients with small cell lung cancer. Part I. Influence of AD on the haemostatic system].

In the last years, a sharp rise in the morbidity due to lung cancer is observed, especially in the male population. Despite the intensive, multidirectional development of oncology, early detection and effective treatment of lung cancer is still limited. Its detection is delayed because of the lack of characteristic early signs.

Biomarkers in various types of atrophic gastritis and their diagnostic usefulness.

Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic gastritis; MAG), resulting in both hypogastrinemia and hypopepsinogenemia I; and rare atrophic gastritis limited to the oxyntic gland area, with antibodies against oxyntic cells and/or intrinsic factor (autoimmune metaplastic atrophic gastritis; AMAG). This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (13C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion.

Duodenal mucosal protection by bicarbonate secretion and its mechanisms.

Proximal portion of duodenum is exposed to intermittent pulses of gastric H(+) discharged by the stomach. This review summarizes the mechanisms of duodenal mucosal integrity, mainly the role of mucus-alkaline secretion and the mucous barrier protecting surface epithelium against gastric H(+). The mucous barrier protects the leaky duodenal epithelium against each pulse of gastric H(+), which penetrates this barrier and diffuses into duodenocytes, but fails to damage them due to; a) an enhanced expression of cyclooxygenase-1 (COX-1), with release of protective prostaglandins (PG) and of nitric oxide (NO) synthase (NOS) with, however, production of NO, stimulating duodenal HCO(3)(-) secretion and b) the release of several neurotransmitters also stimulating HCO(3)(-) secretion such as vasoactive intestinal peptide (VIP), pituitary adenylate-cyclase activating polypeptide (PACAP), acetylcholine, melatonin, leptin and ghrelin released by enteric nerves and mucosal cells.

Neuroendocrinology of gastric H+ and duodenal HCO3- secretion: the role of brain-gut axis.

Gastric H+ and duodenal HCO3- secretions are precisely regulated by neuro-hormonal mechanisms at central and peripheral levels to match the rate of these secretions with the type of stimulation of sensory receptors in the head area (sight, smell, taste, etc.) and in the gastro-intestinal system. Two-way communication pathways operate between the brain and the gut, each comprising afferent fibers signaling sensory information from the gut to the brain and efferent fibers transmitting signals in opposite direction.