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Biomedical subjects

A Tarnawski

Publications and source records attributed to A Tarnawski.

At least 37 records · Page 2Linked to original sources
PubMed1996

Laboratory diagnosis of Helicobacter pylori infection by polymerase chain reaction.

Although the detection of Helicobacter pylori (Hp) infection is important, it is a rather difficult task using only conventional diagnostic techniques. In this study, we have applied a polymerase chain reaction (PCR)-based assay for the diagnosis of Hp infection. RT-PCR for Hp ribosomal RNA was utilized, using the gastric biopsy specimens obtained endoscopically from 10 patients. PCR primers have been designed from the highly consensus region of the 7 different Hp rRNA sequences in GenBank. In the detection of Hp, PCR was more sensitive than culturing and showed 100% of the sensitivity and specificity compared with histology. Our primer pair could detect as few as 50 organisms per reaction. RT-PCR for Hp rRNA is a sensitive and specific method to detect Hp infection in the gastric mucosa.

Base Sequence↗
PubMed1995

Influence of acid and angiogenesis on kinetics of gastric ulcer healing in rats: interaction with indomethacin.

Indomethacin delays healing of experimental gastric ulcers. We investigated whether inhibition of gastric acid secretion by omeprazole or stimulation of angiogenesis by basic fibroblast growth factor (bFGF) may reverse this delay. Rats with gastric ulcers induced by cryoprobe were treated subcutaneously with either placebo, indomethacin (2 x 0.5 mg/kg), bFGF (2 x 100 micrograms/kg), omeprazole (1 x 40 mumol/kg), indomethacin plus omeprazole, or indomethacin plus bFGF given daily for 8, 10, 15, and 22 days. Ulcer size, epithelial cell proliferation, angiogenesis, and maturation of granulation tissue were sequentially quantified. Omeprazole significantly accelerated ulcer healing in an early phase (days 3-8). In contrast, bFGF accelerated healing in a late phase (days 10-15). Indomethacin significantly delayed ulcer healing in late phase and decreased prostaglandin generation, cell proliferation, angiogenesis, and maturation of granulation tissue. Despite stimulation of angiogenesis, bFGF did not reverse indomethacin-induced delay in ulcer healing. In contrast, omeprazole reversed indomethacin-induced effects on angiogenesis, cell proliferation, maturation of granulation tissue, and ulcer healing rate.

Animals↗
PubMed1995

Indomethacin interferes with epidermal growth factor binding and proliferative response of gastric KATO III cells.

Indomethacin induces gastric ulcerations and decreases cell proliferation in the gastric ulcer margin. Since epithelial cell proliferation is under control of epidermal growth factor (EGF), we studied whether indomethacin may affect specific binding of [125I]-EGF to its receptors in cultured human gastric KATO III cells. To assess effects of EGF, indomethacin and their combination on cell proliferation, KATO III cells were incubated for 24 h with either (a) vehicle (b) indomethacin (doses from 10(-5) to 10(-3) M), EGF (doses 0.01, 0.05 or 0.1 microgram/ml) or (d) a combination of b and c, and the bromodeoxyuridine labeling index was determined. Indomethacin in a dose which did not affect cell viability significantly (by 21.5%) decreased [125I]-EGF binding to the KATO III cells and decreased the bromodeoxyuridine labeling index. Epidermal growth factor significantly increased cell proliferation and increased the labeling index from 28.9 +/- 0.6% in the vehicle group to 36.2 +/- 0.5%. Co-treatment with indomethacin significantly reduced the proliferative response of KATO III cells to EGF. In conclusion, indomethacin, in a dose which does not affect cell viability, decreased binding of EGF to cultured gastric KATO III cells and decreased their proliferative response to EGF.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

Cellular and molecular mechanisms of gastric ulcer healing. Is the quality of mucosal scar affected by treatment?

BACKGROUND: Ulcer healing, i.e. the reconstruction of the mucosal architecture, is an active process of filling the mucosal defect with proliferating and migrating epithelial cells and connective tissue. METHODS: This article represents a summary of histologic and ultrastructural assessment of the cellular events occurring during healing of experimental gastric ulcer. RESULTS: Mucosa adjacent to the ulcer crater forms a 'healing' zone. The gastric glands in this zone dilate and the epithelial cells lining these glands de-differentiate, express epidermal growth factor receptor, and proliferate. The latter is the result of local activation of genes encoding for EGF and its receptors. At the ulcer margin, proliferating and dividing epithelial cells migrate onto the granulation tissue to cover (re-epithelialize) the ulcer and bud into granulation tissue to reconstruct glandular structures within the ulcer scar. Re-epithelialization and reconstruction of epithelial structures is under control of epidermal growth factor (EGF) and related peptides which are produced locally by regenerating cells. Under control of fibroblast growth factors, granulation connective tissue grows extensively supplying (a) microvessels for restoration of the microvascular network and (b) connective tissue cells for restoration of the lamina propria within the mucosal scar. The final outcome of the healing process reflects a dynamic interaction between the epithelial component for the 'healing' zone at the ulcer margin and the connective tissue component (including microvessels) originating from the granulation tissue. Depending on these interactions, mucosal scar can be of good quality (restoration close to normal) or poor quality. While a number of pharmacologic agents affect gastric ulcer healing, it is unknown whether these drugs affect the quality of mucosal architecture reconstruction. In previous studies, we demonstrated that sucralfate exerts a trophic effect on gastric mucosa and, compared with omeprazole, improves the quality of restored mucosal structures within the scar of healed gastric ulcers. In the most recent studies, we demonstrated that treatment with sucralfate activates genes for EGF, bFGF, and their receptors, significantly increasing (vs placebo and omeprazole) expression of EGF and its receptor in ulcerated gastric mucosa. CONCLUSION: Thus, the superior quality of ulcer healing by sucralfate (versus omeprazole) is most likely based on its capacity to induce and stimulate expression of EGF, bFGF, and their receptors.

Animals↗
PubMed1995

Quality of gastric ulcer healing. Is it influenced by antiulcer drugs?

BACKGROUND: Chronic administration of sucralfate (SCR), a non-systemic ulcer-healing drug, exerts a trophic action on the gastric mucosa and prevents or reduces ulcer recurrence. The aim of this study was to determine whether SCR and/or the acid inhibiting drug omeprazole (OME) may affect the quality of ulcer healing, i.e., restoration of mucosal architecture. METHODS: Gastric ulcers were produced in male rats by serosal application of acetic acid. Rats were gavaged twice daily for 14 days with 2 ml of: (a) Placebo (PLA), (b) SCR 500 mg/kg, or (c) OME, 50 mg/kg starting 48 h after ulcer induction. We determined ulcer size under a dissecting microscope, and performed quantitative histologic assessment of quality of healing score (QS) on a scale from 0 (normal) to 5 (most abnormal). RESULTS: Ulcer size was 1.4 +/- 0.15 mm in the PLA group, 0.61 +/- 0.1 mm in the SCR group and 0.86 +/- 0.13 mm in the OME group (both OME and SCR p < 0.01 versus PLA). In the PLA group, histology showed (in rats with ulcers) a well-developed ulcer margin with cystically dilated glands. The QS of the ulcer scar in the PLA group was 3.3 +/- 0.22. IN the SCR-treated group, within the scar gastric glands were less dilated, more vertically oriented and the healing zone and granulation tissue were well developed and organized. The QS was 1.6 +/- 0.2, p < 0.001 versus PLA and OME. In the OME group, the ulcer margin and the scar were thinner-reduction of mucosal thickness by 43 +/- 2% (p < 0.005) and 18 +/- 1%, respectively, versus SCR and PLA groups. The number of dilated glands and connective tissue components in the scar was increased by 60%. The QS was 3.6 +/- 0.3. CONCLUSIONS: (1) Both SCR and OME significantly reduced the size of the experimental gastric ulcer. (2) Restoration of mucosal architecture, assessed quantitatively, was much better in the SCR than in the OME and PLA-treated groups. (3) a trophic action of SCR on the gastric mucosa may be the basis of better quality of ulcer healing with SCR.

Animals↗
PubMed1995

The role of extracellular matrix in injury to gastric mucosa by indomethacin.

The extracellular matrix components fibronectin, collagen IV, and laminin provide structural support for the gastric mucosal cells and influence cell migration, attachment, differentiation, and proliferation. Because little is known about the effect of indomethacin on the extracellular matrix, we studied the expression and distribution of extracellular matrix components in the gastric mucosa before and sequentially during indomethacin injury. A total of 32 male Sprague-Dawley rats were treated with placebo or indomethacin 100 mg intraperitoneally. One, 4, and 18 h later, stomachs were excised and gastric specimens were immunostained with specific antibodies against fibronectin (FN), collagen IV (CIV), laminin (LM), fibronectin receptor (FNR), and vimentin (VM). Gross necrosis, quantitative histology, and expression of FN, CIV, LM, FNR, and VM were analyzed using a videoimage analysis system. In the mucosa treated with indomethacin, the expression of VM and LM was decreased by 54% (p < 0.01) and 52% (p < 0.01), respectively, within 1 h vs. control mucosa. The former reflected damage to endothelial cells. Expression of FN, FNR, and CIV was decreased by 50, 25, and 50%, respectively, at 1 h after indomethacin, reflecting significant damage to the extracellular matrix. However, at 1 h, no gross necrosis and no histologic damage were seen in the gastric mucosa. We conclude that expression of extracellular matrix components in the gastric mucosa is significantly reduced during indomethacin injury and that damage to extracellular matrix and microvascular endothelium precedes injury of glandular epithelial cells.

Animals↗
PubMed1995

Cellular mechanisms, interactions, and dynamics of gastric ulcer healing.

An ulcer is a deep, focal defect in the gastric or duodenal wall penetrating through the entire thickness of mucosa and muscularis mucosae. Ulcer healing (i.e., the reconstruction of the muscularis mucosae and mucosal architecture) is an active process of filling the mucosal defect with proliferating and migrating epithelial cells and connective tissue. Mucosa adjacent to the ulcer creater forms a healing zone. Gastric glands in this zone dilate and the epithelial cells lining these glands dedifferentiate, express epidermal growth factor (EGF) receptor, and proliferate. The proliferation is triggered by local activation of genes encoding for EGF and its receptor. From the ulcer margin, proliferating epithelial cells migrate onto the granulation tissue to cover (re-epithelialize) the ulcer and bud into granulation tissue to reconstruct gastric glands in the ulcer scar. Re-epithelialization and reconstruction of epithelial structures are under control of EGF and related peptides produced locally by regenerating cells. Granulation tissue at the ulcer base (whose growth is regulated, at least in part, by fibroblast growth factors) supplies microvessels for restoration of the microvascular network and connective tissue for restoration of the lamina propria within the mucosal scar. The ulcer healing reflects a dynamic interaction between the epithelial component from the healing zone at the ulcer margin and the connective tissue component (including microvessels) originating from the granulation tissue.

Animals↗
PubMed1995

Role of extracellular matrix in attachment, migration, and repair of wounded rabbit cultured gastric cells.

The aim of this study was to determine whether extracellular matrix components affect attachment, proliferation, migration, and repair of wounded rabbit gastric cells in primary culture. Gastric cells were inoculated on culture plates coated without or with collagen type I, type IV, laminin, or fibronectin. The number of attached cells was counted at 3, 5, 24, 48, and 72 h after inoculation. Cell proliferation was assessed with [3H]thymidine incorporation. To assess cell migration and repair after wounding, a confluent monolayer was cut in a standardized manner and the size of the wound area was measured with a computerized analysis system. The number of attached cells increased significantly in plates coated with the extracellular matrix components within 3 h after inoculation. Collagen type I was the most potent stimulator of attachment. Extracellular matrix components did not affect thymidine incorporation. Wound healing was significantly accelerated in the plates coated with collagen type I, type IV, and laminin (70.2 +/- 1.0%, 68.0 +/- 1.0%, and 69.2 +/- 0.9% of initial wound area, respectively, vs. 74.0 +/- 0.6% of initial wound area in controls). Extracellular matrix components play an important role in attachment, migration, and repair of wounded cultured gastric epithelial cells.

Animals↗
PubMed1994

Natural gastric infection with Helicobacter pylori in monkeys: a model for spiral bacteria infection in humans.

BACKGROUND/AIMS: There is no generally accepted model for Helicobacter pylori infection in humans. The aim of this study was to examine the natural history and effect of treatment in rhesus monkeys and sequentially define the immune response to H. pylori in relation to treatment. METHODS: Infection and gastritis were graded blindly by histological analysis and culture of biopsy specimens harvested during gastroduodenoscopies in 26 anesthetized colony-bred monkeys. Plasma H. pylori-specific immunoglobulin (Ig) G levels were determined by enzyme-linked immunosorbent assay. RESULTS: H. pylori and Gastrospirilum hominis-like organisms were present in 13 and 9 monkeys, respectively; 3 animals harbored both organisms, whereas 4 monkeys were not infected. Gastritis score was < or = 1.5 in animals uninfected or infected only with G. hominis-like organisms and > or = 2.0 in all H. pylori-infected animals. IgG ratios were > or = 0.5 in 12 of 13 H. pylori-infected animals and in 2 of 13 H. pylori-negative animals (P < 0.001). One monkey became infected with H. pylori during the observation period, with concurrent increase of gastritis and plasma IgG levels. In untreated animals, infection, gastritis, and plasma IgG levels remained unchanged over 7-15 months. Triple therapy eradicated H. pylori at 6 months in 4 of 6 animals while suppressing gastritis and plasma IgG levels. CONCLUSIONS: Rhesus monkeys harboring H. pylori are persistently infected and have gastritis and elevated specific IgG levels, all of which may respond to appropriate therapy, whereas G. hominis infection is associated with little inflammation.

Animals↗
PubMed1994

Distorted microangioarchitecture and impaired angiogenesis in gastric mucosa of portal hypertensive rats.

BACKGROUND/AIMS: Portal hypertensive (PHT) gastropathy is now recognized as a distinct entity, but the size of microvessels has been a subject of controversy. Angiogenesis in PHT gastric mucosa has not been explored. The aim of this study was to examine the angioarchitecture of PHT and non-PHT gastric mucosae before and after ethanol-induced injury utilizing microvascular cast techniques. METHODS: Portal hypertension was produced by staged portal vein occlusion. Fourteen days later, gastric vascular casts were made in both PHT and control (sham-operated) rats by Mercox resin infusion. After tissue dissolution, casts were examined under a scanning electron microscope. To examine angiogenesis in injured gastric mucosa, the above study was repeated in PHT and control rats 18 hours after intragastric administration of 100% ethanol. RESULTS: The capillary casts in PHT gastric mucosa (mean diameter, 6.3 +/- 0.03 microns) were significantly narrower than those of controls (mean diameter, 8.6 +/- 0.02 microns; P < 0.01). After ethanol injury, 5.5% +/- 0.3% of microvessels in gastric mucosa of sham-operated rats contained buds, showing angiogenesis. In contrast, PHT gastric mucosa had a paucity of capillary angiogenesis (buds in only 0.4% +/- 0.2% of microvessels; P < 0.01 vs. control). CONCLUSIONS: This study shows prominent persistent abnormalities in the microangioarchitecture of PHT gastric mucosa. Moreover, PHT gastric mucosal microvessels have a marked impairment of angiogenic response to ethanol injury.

Animals↗
PubMed1994

Epidermal growth factor induces biphasic activation of ornithine decarboxylase in human stomach-derived KATO-III cells.

Effect of epidermal growth factor (EGF) on ornithine decarboxylase (ODC) was examined in human gastric cancer-derived KATO-III cells, because 125I-EGF binding studies indicated a presence of specific binding sites for EGF on these cells. Upon stimulation with EGF, both ODC mRNA expression and ODC enzyme activity were significantly increased in KATO-III cells. However, unlike in other cellular systems, both EGF-induced ODC mRNA expression and ODC enzyme activation were biphasic with the peaks at 15 +/- 10 min and 2.1 +/- 1.5 hrs (mean +/- SE) for mRNA, and 3.1 +/- 1.5 and 7.7 +/- 1.8 hrs (mean +/- SE) for enzyme activity, respectively. Therefore, KATO-III cell line may provide a unique model for the biochemical analysis of EGF action on ODC activation.

Cell Line↗
PubMed1994

Antacid provides better restoration of glandular structures within the gastric ulcer scar than omeprazole.

Mucosa of healed gastric ulcers displays histological abnormalities that are possibly the basis of ulcer recurrence. The influence of antacid and omeprazole treatment was studied on the quality of ulcer healing. Sixty four rats with gastric cryoulcers were treated daily either with placebo, antacid, omeprazole, or antacid plus omeprazole. Ulcer size was measured three times per week with a novel video endoscopic method. Prostaglandin generation (day 6), cell proliferation (day 8 and 15), height and cell composition of ulcer margin (day 8), and mucosal scar (day 15) were quantitatively assessed. Antacid, omeprazole, and antacid plus omeprazole significantly accelerated ulcer healing predominantly during days 3-8. Compared with placebo, the height of ulcer margin and mucosal ulcer scar was significantly increased in antacid (+7 and +9% respectively) and significantly decreased in omeprazole (-33 and -22% respectively) and antacid plus omeprazole (-26 and -18% respectively) treated rats. The number of bromodeoxyuridine labelled cells (+42%, day 8), epithelial cell mass (+42%, day 15), and the ratios of epithelial cells/connective tissue (+73%, day 15) and epithelial cells/gland lumen (+100%, day 15) were significantly increased in antacid treated rats. In conclusion, both antacid and omeprazole accelerate ulcer healing but antacid provides a better quality of healing. This advantage is lost by cotreatment with omeprazole.

Aluminum Hydroxide↗
PubMed1993

Increased susceptibility to injury and normal reactivity to prostaglandin protection of mucous cells isolated from gastric mucosa of portal hypertensive rats.

We examined the susceptibility of mucous cells isolated from gastric mucosa of portal hypertensive rats to ethanol injury. In addition, we assessed their response to protective action of prostaglandin against ethanol injury in vitro. Ethanol significantly decreased cell viability in calcium-containing medium. The injury of mucous cells isolated from portal hypertensive rats was more extensive than those isolated from sham-operated rats. Ethanol-induced cell injury was reduced similarly in both groups by pretreatment with 16,16-dimethyl prostaglandin E2. These results suggest that mucous cells isolated from portal hypertensive gastric mucosa are more susceptible to ethanol injury and this susceptibility is dependent on extracellular calcium. The cells from portal hypertensive gastric mucosa retain, however, sensitivity to protective action of 16,16-dimethyl prostaglandin E2.

16,16-Dimethylprostaglandin E2↗
PubMed1993

Epidermal growth factor protects gastric mucosa against ischemia-reperfusion injury.

Epidermal growth factor (EGF) protects gastric mucosa against many injurious factors, but no study has examined whether EGF may protect against ischemia-reperfusion (I-R)-induced gastric mucosal injury. We assessed the effect of EGF pretreatment on the extent of ischemia-reperfusion-induced gastric mucosal damage in rats. Assessment of injury and protection included: the extent of macroscopic necrosis; qualitative and quantitative histology with measurement of deep mucosal necrosis; microvascular permeability after injection of fluorescein-conjugated albumin; and transmission electron microscopy. After I-R, saline-pretreated rats (placebo group) had macroscopic necrosis involving 40 +/- 6% of total gastric mucosal area. Histology revealed exfoliation of the surface epithelial cells, mucosal hemorrhages, microvascular injury, and extensive deep mucosal necrosis involving 7 +/- 5% of mucosal strips. Microvascular permeability assessed by fluorescein-conjugated albumin was significantly increased to 327 +/- 29% of that in normal rats (without ischemia-reperfusion). Transmission electron microscopy showed severe microvascular injury. EGF pretreatment significantly reduced gross mucosal necrosis to 17 +/- 6% and deep histologic mucosal necrosis to 2 +/- 1% (both p < 0.01 versus saline pretreated). Integrity of the mucosal microvessels was preserved and microvascular permeability was close to normal. This study demonstrates that EGF significantly reduces ischemia-reperfusion injury to the rat gastric mucosa and that this effect of EGF may be mediated by its protection of the mucosal microvessels.

Animals↗
PubMed1993

Goiter incidence and urinary iodine excretion in children of age group 6-13 years living in south-eastern Poland (Kraków coordinating center).

The study included 4103 school children attending randomly selected schools localized in towns and villages of 3 geographically distinct regions: mountainous, (Carpathian endemia), upland, lowland. The children were divided into four age-related groups. The incidence of goiter as detected by palpation was 38.1% in all the children studied, the value being similar in all three regions (38.1, 37.3 and 38.6%, respectively). Goiter incidence differs slightly among urban and rural children, amounting to 40.5 and 34.5%, respectively, in the two groups. In about 60% of children urinary iodine excretion was lower than 50 micrograms/l, while in about 30% it was normal. In about 10% of children studied urinary iodine excretion was lower than 20 micrograms/l. The results obtained indicate the occurrence among children of the studied region of goiter endemy of moderate degree. It was found that the percentage of children excreting more than 50 micrograms/l of urinary iodine was higher among those consuming iodized salt as compared to those consuming non-iodized salt. The first effects of resumption of common salt fortification with iodide in southern Poland can already be noted. There is, however, a need for optimization and steady control over this prophylactic action.

Adolescent↗
PubMed1993

Apoptosis: genetically programmed physiologic cell loss in normal gastric oxyntic mucosa and in mucosa of grossly healed gastric ulcer.

Maintenance of gastric mucosal structure depends on a dynamic balance between cell loss and cell renewal. The surface epithelial cells exfoliate at a rapid rate (usually in response to luminal contents) and are entirely replaced within 3-5 days. The loss of parietal, chief, and endocrine cells is much slower, but there is little information concerning the morphologic aspects of this process. Because in other tissues cells are physiologically eliminated through a process of apoptosis--genetically programmed cell self-destruction and loss--we studied whether this process occurs in normal gastric mucosa and in the mucosa of recently healed gastric ulcers in the rat. Degeneration and loss of the surface epithelial cells into the gastric lumen occurs in normal oxyntic mucosa, and more extensive desquamation of poorly differentiated mucous cells in the dilated gastric glands takes place within mucosal scars of grossly healed gastric ulcers. Apoptosis of parietal, chief, and endocrine cells in normal oxyntic mucosa and apoptosis of poorly differentiated cells lining dilated glands in mucosal scar were assessed and characterized by electron microscopy. Apoptosis affects single glandular cells and involves a rapid initial condensation of both nucleus and cytoplasm, with subsequent fragmentation. Finally, the cell is converted into a cluster of membrane-bound apoptotic bodies, which usually are engulfed by adjacent cells or disposed into a glandular lumen. Desquamation of surface epithelium and apoptotic self-destruction of glandular epithelium stimulate a constant cell renewal and thus contribute to the maintenance of the ulcer healing process. Rapid and "excessive" proliferation of regenerating gastric epithelium enables re-epithelialization of ulcer crater.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1993

Inhibitory effects of indomethacin on growth and proliferation of gastric carcinoma cells KATO III.

The effects of indomethacin on growth and proliferation of gastric carcinoma cells KATO III were examined. Indomethacin (10(-4) and 10(-3) M) significantly inhibited cell growth and these effects were not affected by treatment with 16,16-dimethyl prostaglandin E2 (3 x 10(-7) M and 3 x 10(-6) M). Indomethacin 10(-3) M significantly reduced cell viability and completely inhibited cell growth. Indomethacin 10(-4) M did not affect cell viability and its inhibitory effect of cell growth became apparent on the fifth day of culture. Indomethacin 10(-4) M reduced BrdU labeling index within 2 hours. These results suggest that indomethacin inhibited growth and proliferation of gastric carcinoma cells KATO III. This effect is not mediated by prostaglandins.

Antineoplastic Agents↗