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Biomedical subjects

V P Kalinovskiĭ

Publications and source records attributed to V P Kalinovskiĭ.

At least 19 recordsLinked to original sources
PubMed2006

[Chronic atrophic gastritis: morphological features and pepsin formation function].

The paper discusses a modern approach to chronic atrophic gastritis as a precancerous gastric condition. It deals with the role of Helicobacter pylori infection, development of disease, morphological changes taking place in gastric mucosa associated with chronic atrophic gastritis, and their importance for gastrocarcinogenesis. Recommendations are given on the strategies of management of precancerous gastric changes in mucosa as well as early prophylaxis of stomach cancer development from chronic atrophic gastritis associated with Helicobacter pylori infection.

Adult↗
PubMed2004

[Study of the antioxidant drug "Karinat" in patients with chronic atrophic gastritis].

A randomized double blind placebo-controlled trial of the drug karinat was carried out in patients with chronic multifocal atrophic gastritis. Karinat contains beta-carotene 2.5 mg, alpha-tocopherol 5 mg, ascorbic acid 30 mg and garlic powder 150 mg per tablet. Out of 66 patients, 34 received karinat, 32--placebo. Both karinat and placebo were administered for 6 months, one tablet twice a day. Karinat therapy improved digestion, the fibrogastroscopic pattern of mucosa, inhibited Helicobacter pylori infection, stimulated stomach activity, mitigated intestinal metaplasia and interfered with the epithelial proliferation of gastric mucosa. These therapeutic effects were more pronounced in the study group. On the whole, the effectiveness of the drug was significantly higher (29%). Karinat should be recommended for the management of chronic atrophic gastritis, a precursor of stomach cancer.

Anticarcinogenic Agents↗
PubMed2000

[Radioimmunoassay of serum pepsinogen I in chronic gastritis and stomach cancer].

Blood serum in stomach cancer and chronic gastritis has been compared. A sharp decrease in pepsinogen 1 level both in cancer and gastritis patients was found as compared with healthy subjects. Pepsinogen 1 level in poorly-differentiated tumor (37.4 ng/ml) was lower than in well-differentiated one (58.2 ng/ml).

Chronic Disease↗
PubMed1999

[Evaluation of pepsinogen A expression in stomach cancer].

The report deals with a molecular-genetic study of human pepsinogen A (PGA) genetic locus. EcoRI, HindIII and BamH 1 restriction endonuclease technique were employed. The investigation involving 58 patients with stomach cancer (SC) and 18 healthy donors failed to identify any significant PGA genetic restructuring in the blood of healthy donors. However, DNA sampled from tumor tissue showed lower expression and deletion of PGA fragments as compared with those of unaltered gastric mucosa in the same patients. Such changes were identified in 27 SC patients.

Case-Control Studies↗
PubMed1998

[Biochemical and immunologic analysis of pepsinogen I in blood serum and mucosa in patients with gastric tumors and non-tumor diseases].

The results of the biochemical and immunologic studies of pepsinogen I (PG-I) occurring in the mucosa and blood serum of patients with tumors and non-tumor conditions of the stomach are discussed. Pepsinogen I was identified in human blood serum using rabbit antibodies against PG-I. Sharp drop in blood serum-PG-I level in patients with gastric tumors has been confirmed.

Gastric Mucosa↗
PubMed1998

[Microsatellite instability of genome in cells of sporadic and hereditary carcinoma of the gastrointestinal tract].

Microsatellite instability (MIN) of human genome, i.e. instability of very short (1-5 nt) DNA tandem repeats, points to a deficiency in the mismatch repair system (MMR). To investigate the role of MMR in sporadic and hereditary carcinogenesis in the gastrointestinal tract, four types of carcinomas were compared: sporadic (GC), familial (FGC) gastric carcinoma, sporadic colorectal (CC) and hereditary nonpolyposis colorectal (HNPCC) carcinoma. No significant difference in MIN frequency was found between GC (9 out of 27) (33%) and CC (7 out of 29) (24%). In hereditary carcinoma group, MIN occurrence appeared 2-3 times as high: FGC in 7 out of 10 (70%) and HNPCC in 6 out of 8 patients (75%). No significant differences were recorded in MIN occurrence at early and later stages of the disease in all groups. Therefore, it can be suggested that disorders in the MMR develop at earlier stages of carcinogenesis and may be responsible for tumor progression.

Base Sequence↗
PubMed1994

[Characteristics of enzymatic function of the stomach in gastroduodenal diseases in children with regard to gastric carcinogenesis].

The paper deals with a description of the biochemical properties of the isoforms of pepsinogen pepsin of gastric mucosa and blood serum in children suffering from duodenal ulcerative disease as well as in atrophic and subtrophic lesions of gastric mucosa. Atrophic gastritis was found to involve an inhibited biosynthesis of the Ist fraction of pepsinogen while ulcerative-erosive lesions of the gastro-duodenal area--an increased level of the 3rd isoform of pepsinogen.

Adolescent↗
PubMed1993

[The use of the 5'PstEJ6.6 probe containing a Ha-ras oncogene promoter in population genetics research by DNA fingerprinting].

The Mendelian inheritance of population genetic markers according to their zygosity has been established in a population investigation carried out in Kazakhstan and the northwestern region of Russia, using the 5'PstEJ6.6 DNA probe genetic variability both for persons of different nationality in a population and between two distant populations has been observed. Said procedure has proved more acceptable than the M13 phage DNA test for mass screening examinations because it involves genome analysis on the basis of DNA markers common to each population.

Adult↗
PubMed1989

[Proto-oncogene expression in the organs of intact adult rats].

The study is concerned with the expression of src, sis, fos, myc, Ha-ras, Ki-ras, N-ras, mos, and abl proto-oncogenes in the brain, heart, liver, kidneys, lung, stomach, cross-striated muscle cells and in leukocytes. Some of these genes are shown to be actively transcribed in adult intact rats. Their expression depends on the tissue specificity. Most of the investigated proto-oncogenes are expressed in the liver and kidney weakly, and in the brain and heart--more strongly. A correlation is observed between fos and Ha-ras proto-oncogenes' expression in organs of intact rats.

Animals↗