[Prevalence and characteristics of clinical manifestations of gastroesophageal reflux disease in the Republic of Mordovia (according to the "Megre" study)].

In the article are shown the results of the study being the first of the detailed population-based study of the prevalence of gastroesophageal reflux disease in Russia based on the reflux questionnaire Mayo Clinic. The high prevalence of gastroesophageal reflux disease was determined among the inhabitants of Saransk. We made the comparative analysis of the symptoms of the disease with regard for sex and age of the respondents.

[Dysbiotic manifestations during eradication therapy of Helicobacter pylori and their corrections].

Forty-eight patients with duodenal peptic ulcer disease infected with Helicobacter pylori were examined. All patients undergo conventional 1-week eradication therapy. After its ending the patients were randomized to two groups: those who will be treated by synbiotics or control group. Normoflorin B and Normoflorin L, which contain bifidobacteria or lactobacilli in complex with different microelements, vitamins, aminoacids, organic acids, and antioxidants, were used as synbiotics. Morphologic study of biopsy samples of small intestine mucosa were performed in patients from both groups. It was determined that eradication therapy worsened existing symptoms of dyspepsia in 80.9% of cases or lead to their emergence, connected with dysbiotic manifestations, in 55.5% of patients. Inclusion of synbiotics in complex therapy resulted in rapid and effective elimination of dyspeptic symptoms, promoted recovery of affected morphologic and functional states of small intestine mucosal epithelium, and optimized metabolic processes important for the digestion.

Evidence for contribution of an internal ribosome entry site to intercellular transport of a tobamovirus.

Previously, it has been shown that tobacco mosaic virus (TMV) U1 and crucifer-infecting TMV contain a 75 nt internal ribosome entry site (IRES) upstream of movement protein (MP) gene (IRES(U1)(MP,75) and IRES(CR)(MP,75), respectively). A movement-deficient TMV mutant, KK6, has been constructed previously [Lehto, K., Grantham, G. L. & Dawson, W. O. (1990). Virology 174, 145-157] by insertion of the second coat protein subgenomic promoter (CP SGP-2) upstream of the MP gene, in addition to the natural CP SGP-1. Here, the authors compare the efficiency of movement function expression by KK6 and a derivative, K86, obtained by insertion of IRES(CR)(MP,75) between the CP SGP-2 and MP genes resulting in restoration of IRES(CR)(MP,75) function in the 5'-untranslated sequence of the I(2) subgenomic RNA of K86. The data indicate that the efficiency of K86 movement was largely restored by this insertion, which was apparently due to the translation-enhancing ability of IRES(CR)(MP,75).

Normal postprandial lipemia and chylomicron clearance in offspring of parents with early coronary artery disease.

To assess the importance of postprandial lipemia and delayed chylomicron clearance as early atherogenic risk factors, 60 male offspring of parents with early coronary artery disease (CAD) and 41 controls were administered a fat-rich meal containing vitamin A. There were no significant differences between CAD-positive (CAD+) offspring and CAD-negative controls for areas under the postprandial curves for triglyceride and plasma, chylomicron, and chylomicron remnant retinyl palmitate. Older CAD+ offspring, aged 31-45 yr, had significantly increased very low density lipoprotein (VLDL) cholesterol, VLDL triglyceride, VLDL apoprotein B, and areas under postprandial curves for triglyceride and plasma, chylomicron, and chylomicron remnant retinyl palmitate than younger CAD+ offspring, aged 15-30 yr. Correcting for waist/hip ratio eliminated significant differences between the two groups for VLDL and areas under the triglyceride and chylomicron remnant curves, but this was not the case for the insulin sensitivity index. We conclude that neither increased postprandial lipemia nor abnormalities of chylomicron clearance are important early atherogenic risk factors in this population. An increase in age is associated with increased VLDL and postprandial lipemia and decreased chylomicron remnant clearance. This is due mainly to an increase in the waist/hip ratio and not to a change in insulin sensitivity.

Insulin resistance is not a major determinant of low-density lipoprotein particle size.

The relationship between low-density lipoprotein (LDL) peak particle diameter and insulin sensitivity, very-low-density lipoprotein (VLDL) + intermediate-density lipoprotein (LDL) triglyceride, cholesterol, and apoprotein B, postprandial lipemia, and LDL + high-density lipoprotein (HDL) triglyceride was assessed. The subjects were 101 healthy males aged 15 to 45 years. Sixty-one subjects (60.4%) were offspring of a parent with coronary artery disease before age 60, and 40 subjects (39.6%) had no parental history of coronary artery disease. LDL peak particle diameter was measured following polyacrylamide gradient gel electrophoresis. An insulin sensitivity index (Si) was determined from a frequently sampled intravenous glucose tolerance test using a minimal modeling method. A fat tolerance test was performed with a test meal containing 70 g/m2 fat, with triglyceride concentrations measured hourly for 12 hours. LDL peak particle diameter was significantly correlated with body mass index (BMI) (r = -.282, P < .01), waist to hip ratio (r = -.291, P < .01), fasting triglyceride (logarithmically [log] transformed) (r = -.566, P < .001), area under the postprandial triglyceride curve (log transformed) (r = -.562, P < .001), VLDL + IDL triglyceride (log transformed) (r = -.462, P < .001), VLDL + IDL cholesterol (log transformed) (r = -.477, P < .001), VLDL + IDL apoprotein B (log transformed) (r = -.321, P < .001), LDL + HDL triglyceride (log transformed) (r = .583, P < .001), and HDL cholesterol (r = .347, P < .001), but there was no significant correlation with Si. Using stepwise regression analysis, LDL + HDL triglyceride showed the strongest relationship to LDL peak particle diameter, accounting for 34% of the variation in size. Si was not an independent predictor of LDL particle size. In conclusion, insulin sensitivity appears to have little influence on LDL particle size. The importance of LDL + HDL triglyceride should be considered a preliminary finding warranting verification in this and other populations.

Low-density lipoprotein particle size is not a discriminating marker for atherogenic risk in male offspring of parents with early coronary artery disease.

The aim of this study was to assess the importance of low-density lipoprotein (LDL) particle size as a marker of atherogenic risk in male offspring of a parent with early coronary artery disease (CAD) before the age of 60 years. CAD-positive (CAD+) offspring were recruited into two groups based on age, 15 to 30 years (n = 20) and 31 to 45 years (n = 41), and matched to CAD-negative (CAD-) offspring by age and body mass index (BMI) (n = 20 and 21 per group). LDL peak particle diameter was assessed by polyacrylamide gradient gel electrophoresis. There was no significant difference in LDL peak particle diameter between CAD+ and CAD- offspring (26.2 +/- 0.1 v 26.2 +/- 0.1 nm, mean +/- SE). There was also no difference between CAD+ offspring and CAD- offspring when comparisons were made within their own age group (26.5 +/- 0.1 nm in younger CAD+ offspring v 26.2 +/- 0.1 nm in younger CAD- offspring, and 26.0 +/- 0.1 nm in older CAD+ offspring v 26.1 +/- 0.2 nm in older CAD- offspring). Peak particle diameter was significantly greater in younger CAD+ offspring than in older CAD+ offspring (26.5 +/- 0.1 v 26.0 +/- 0.1 nm, P < .05). We conclude that small LDL particle size is not a discriminating marker for early atherogenic risk, and that measurement of LDL particle size has limited value in the assessment of coronary risk, at least in the age ranges we studied.

Decreased glucose tolerance, not decreased insulin sensitivity, is a maturational abnormality in the male offspring of a parent with early coronary artery disease.

We investigated whether the male offspring of a parent with early coronary artery disease (before the age of 60; n = 61) exhibit decreased insulin sensitivity compared with controls matched for age and body mass index (BMI) (n = 39). The insulin sensitivity index (S[I]) was determined by the minimal modeling method of Bergman from a frequently sampled intravenous glucose tolerance test with intravenous tolbutamide. Offspring and controls had a similar S[I], insulin-independent glucose utilization (S[G]), first-phase insulin response (AIR[G]), and area under the glucose curve. When subjects were separated into two age groups, younger subjects aged 15 to 30 years and older subjects aged 31 to 45 years, important differences were seen. S[G] was significantly increased in younger offspring compared with controls (22.8 +/- 2.3 v 16.8 +/- 2.3 x 10(-3) x min(-1), P < .05). Older offspring had a significantly increased area under the glucose curve compared with controls (18,250 +/- 322 v 17,225 +/- 347 mg/dL x min(-1), P < .05). Older offspring also had decreased S[I] compared with younger offspring (5.0 +/- 0.4 v 6.6 +/- 0.9 x 10(-4) x min(-1) x micro U/mL, P < .05), but this difference was eliminated after adjusting for BMI and waist to hip ratio (5.5 +/- 0.4 v5.8 +/- 0.9 x 10(-3) x min(-1), nonsignificant). This study does not support the concept that insulin resistance is an early atherogenic risk factor in offspring at risk for coronary disease because of their family history. However, it does point to the importance of maturational changes in glucose homeostasis in these offspring.

[The frequency of chromosome aberrations in the lymphocytes of children with thyroid diseases living in Bryansk Province]. / Chastota aberratsii khromosom v limfotsitakh detei s zabolevaniiami shchitovidnoi zhelezy, prozhivaiushchikh v Brianskoi oblasti.

The number of unstable chromosome aberrations was determined in peripheral blood lymphocytes from 15 children with thyreopathology living in Klintsy (Bryansk Province); the mean age was 14 years. The number of dicentric chromosome is determined to be (0.18 +/- 0.07) per 100 cells and is significantly higher than that in cells from healthy children of Klintsy and Moscow (control). There was no differences in the frequency of other types of chromosome aberrations as well as of aberrant cells.

[The cytogenetic examination of different groups of children living in regions of Bryansk Province contaminated as a result of the Chernobyl accident]. / Tsitogeneticheskoe obsledovanie razlichnykh grupp detei, prozhivaiushchikh v raionakh Brianskoi oblasti, zagriaznennykh v rezul'tate Chernobyl'skoi avarii.

The frequency of chromosome aberrations (CA) was studied in peripheral blood lymphocytes from healthy children and children with thyreopathology living in the city of Klintsy, Bryansk Province (contamination level up to 5 Ci/km2), and two Moscow groups, respectively. We have observed the elevated number of dicentrics and acentric fragments in cell from children with thyreopathology with respect to those from healthy children living in Klintsy. This fact cannot be explained by influence of disease because there was no difference in cytogenetical markers between the groups of healthy children and children with thyreopathology from Moscow. The number of dicentrics was increased in cells from children with high level of internal contamination (more than 400 nCi) living in Krasnaya Gora (15-40 Ci/km2). It is proposed that the internal irradiation is more important for the CA induction. The symmetrical translocation analysis using the method of fluorescence in situ hybridisation (FISH) has shown the absence of this type of aberrations in cells from children with high level of internal irradiation whereas the translocations frequency in cells from control children was (1.1 +/- 0.4) per 1000 cells.

[An evaluation of the radioprotective action of antioxidants on normal human cells and in genomic diseases by using different cytogenetic tests]. / Otsenka radiozashchitnogo deistviia antioksidantov na kletki cheloveka v norme i pri bolezniakh genoma s pomoshch'iu razlichnykh tsitogeneticheskikh testov.

In studying the radioprotective action of natural and synthesised antioxydants a decreased yield of chromosome aberrations with respect to those in untreated cells was noted in normal cells irradiated in phase G1 whereas no radioprotective effect was found in cells irradiated in G0. The addition of antioxydants into the cell cultures from patients with Turner's syndrome did not change their radiosensitivity. No adaptive response was induced in lymphocytes from patients with Down's syndrome cultivated with vitamin E.

Adaptive response in irradiated human lymphocytes: radiobiological and genetical aspects.

The adaptive response (AR) in human lymphocytes in different experimental protocols was investigated. The AR was found to be present in cells pre-exposed to 3 cGy of X-rays in G0, G1 and S phase as well as with tritiated water (4 muCi/ml) when the 'challenge' dose was given in G2. There was no AR after prior exposure of the cells in S phase to secondary irradiation from 70 GeV protons. The AR was not observed after preliminary X-irradiation of the lymphocytes in G0 and G1 and 'challenge' irradiation in G1. Cells from 6 patients with Down's syndrome were tested. At least 5 of them did not show the AR. The AR is considered to be a phenomenon of the antimutagenic aftereffect.

[Absence of radiation-induced adaptive response in lymphocytes of patients with Down's syndrome]. / Otsutsvie radiatsionno-indutsirovannogo adaptivnogo otveta v limfotsitakh bol'nykh s sindromom Dauna.

The adaptive syndrome and response (AR) in lymphocytes from 6 patients with Down syndrome (DS) were investigated. No AR was found to occur in all cases in DS cells pre-exposed to 3 rad of X-rays in S phase of cell cycle and then irradiated with 150 rad of gamma rays in G2 whereas the chromosome aberrations yield in cells from control donors was decreased twice under such conditions of the experiment.