Stages of the cerebral mechanisms of deceptive responses

Cerebral mechanisms of perceiving and telling lies were studied by recording event-related potentials (ERPs) both after an actual deceptive response and during the time interval when the subject decided to tell a lie. Ten healthy volunteers participated in the study. The test consisted of their playing a game against a computer. The subjects could choose between deceptive and truthful answers so as to win the game. The subjects gave a deceptive answer intentionally, the structure of the test ensuring equal numbers of deceptive and truthful answers. The relaxation times in the cases of truthful and deceptive answers did not differ significantly from each other. The comparison of ERPs accompanying deceptive and truthful answers showed the existence of a negativity with a latent period of 90 ms in the regions of the right frontal, central, and right parietal derivations. This negativity indicated that the brain reacted to a deceptive answer even if this a priori “erroneous” act ensured reaching the goal and, in this sense, was subjectively relevant. In terms of the cerebral error detector mechanism, this phenomenon may be regarded as a special case of a general response of the brain to giving an incorrect (deceptive) answer, rather than a response to a lie per se. The interval of time when, presumably, the decision on a deceptive answer was being made was found to contain the late positive component P540, which is most likely to be involved in the preparation of the deceptive answer and the intention to tell a lie.     

The brain mechanism of error detection: the P.E.T. study

In present research, the brain maintenance of the error detection mechanism was studied in resting condition and while subjects consciously implemented incorrect actions (i.e. deception). Assessment of the regional cerebral blood flow revealed involvement of anterior cingulated cortex in deception. The obtained data indicate that it is impossible to consciously control the activity of the error detection mechanism. PET study of patients with obsessive compulsive disorder in resting condition revealed a decrease of brain glucose metabolism in the anterior cingulated cortex in comparison with healthy subjects. These data pointed to malfunctioning of the error detection mechanism. The findings support the formerly proposed hypothesis about the impact of the error detection mechanism in formation and support of obsessive compulsive disorder.     

Development to the blastocyst stage of immature pig oocytes arrested before the metaphase-II stage and fertilized in vitro

In vitro fertilization (IVF) and embryonic development of mature and meiotically arrested porcine oocytes were compared in the present study. After in vitro maturation (IVM) of cumulus-oocyte complexes for 48 h, 75.4% of them extruded a visible polar body (PB). Most of the oocytes with a first polar body (PB+ group) were at the metaphase-II (M-II) stage (91.4%). Most of the oocytes without a visible polar body (PB− group) appeared to be arrested at the germinal vesicle (GV) (41.6%) and metaphase-I (M-I) (34.0%) stages. After IVF of oocytes (day of IVF = Day 0), there was no difference between PB⁺ and PB⁻ groups in rates of sperm penetration, mono-spermy, however oocyte activation rate after penetration was greater in the PB+ than in the PB− group (P < 0.05). On Day 2, there was no difference between rates of embryos cleaved at the 2–4 cell stages in PB+ and PB− groups (42.1 ± 48.8% and 33.6 ± 2.1%, respectively). On Day 4, the rate of PB+ embryos developing beyond the 4-cell stage was greater than that of PB− embryos (P < 0.05, 31.7 ± 3.9% and 14.1 ± 1.5%, respectively), and PB+ embryos had more cells than the PB− embryos (P < 0.05, 8.3 ± 0.4 and 6.0 ± 0.8 cells, respectively). On Day 6, a greater proportion of PB+ embryos developed to the blastocyst stage than did PB− embryos (P < 0.05, 34.6 ± 2.4% and 20.7 ± 2.8%, respectively). However, when the GV oocytes of the PB− group were not included in recalculations, there was no difference in blastocyst rates between M-I arrested and M-II oocytes (35.3 and 34.6%, respectively). The number of blastomere nuclei in embryos obtained from the PB+ group (52.0 ± 2.5) was greater than that from the PB− group (P < 0.05, 29.1 ± 2.8). The proportion of degenerated parts in the blastocysts, as determined by morphological appearance, was the same in the PB+ and PB− groups. Although the quality of PB+ embryos was enhanced as compared with that of the PB− group, the proportion of inner cell mass and trophectoderm cells in PB+ and PB− blastocysts did not differ (1:1.9 and 1:2.2, respectively). Chromosome analysis revealed that PB+ blastocysts had more diploidy (P < 0.05, 69.7%) than did PB− blastocysts (44.0%), whereas PB− blastocysts had more triploid cells (P < 0.05, 34.0%) than did PB+ oocytes (8.4%). These results indicate that pig oocytes arrested before the M-II stage (M-I oocytes) undergo cytoplasmic maturation during maturation culture and have the same ability to develop to blastocysts after IVF as M-II oocytes, but some of them resulted in degeneration or delayed development with poor embryo quality.     

Frequency of mutant lymphocytes in T-cell receptor locus as a possible predictor of thyroid cancer development in irradiated and unirradiated persons

Was compared frequency of lymphocytes mutant at loci of T-cell receptor (TCR) from samples of peripheral blood taken from 186 healthy donors and 46 untreated thyroid cancer patients, including the persons exposed to ionizing radiation as a result of inhabitation in radioactive polluted region of Russian Federation. Was shown that the cell mutation rate within thyroid cancer group was significantly higher than the same parameter for the healthy person with similar age distribution (p < 0.01). It could be a result of such factors as genotoxic influence, different sensitivity or possible genome instability (including radiation-induced). It was found that 37% of patients have the increased frequency of somatic mutation cells, i.e. it exceeded 95% confidence interval for the screening group. The presented results cause to anticipate that TCR-test could be used as one of criteria for formation groups of high cancer risk development.     

Role of Reactive Oxygen Species in the Sensitivity of Rat Hypertrophied Myocardium to Ischemia

The relationship between hydroxyl radical (OH*) generation in the zone of ischemia/reperfusion and the size of infarction formed was investigated in 18-22-week-old anaesthetized male SHRSP and Wistar rats using a myocardial microdialysis technique. The marker of OH* generation, 2,3-dihydroxybenzoic acid (2,3-DHBA), was analyzed in dialyzates by high performance liquid chromatography with electrochemical detection. Myocardial ischemia was induced by ligation of the descending branch of the left main coronary artery for 30 min. The mean value of basal 2,3-DHBA level in the dialyzate samples from SHRSP (243 +/- 21 pg for 30 min) was significantly higher than that from Wistar rats (91 +/- 4 pg for 30 min, p < 0.0002); it positively correlated with left ventricular hypertrophy (r = 0.806; p < 0.05). During reperfusion total 2,3-DHBA output was 1.8-fold higher in SHRSP than in Wistar rats (659 +/- 60 pg versus 364 +/- 66 pg for 60 min, respectively, p < 0.0002). At the same time, 2,3-DHBA increase above the basal level was the same in Wistar and SHRSP rats (181 +/- 25 and 172 +/- 36 pg for 60 min, respectively). The infarct size in SHRSP (45.4 +/- 4.3%) was significantly higher (p < 0.05) than in Wistar rats (32.8 +/- 3.3%). There was a significant positive correlation between basal level of 2,3-DHBA and total reperfusion 2,3-DHBA content in SHRSP (r = 0.752; p < 0.05). Thus, data obtained clearly indicate that the hypertrophied myocardium of SHRSP was less tolerant to ischemia/reperfusion than that of Wistar rats due to chronically increased OH* production and enhanced total OH* output during reperfusion. Greater myocardial damage in SHRSP than in Wistar rats following the equal increase in OH* production above the basal level suggests the existence of deficit of the antioxidant defense in the hypertrophied myocardium.     

The vegetative state as a manifestation of a stable pathological state

The results of comprehensive monitoring of the state of 25 patients in the vegetative state (prolonged coma) before and after compensating for the factors of secondary brain damage were analyzed and followed up for no less than six months. The primary results showed that the best recovery of consciousness and cognitive functions was observed if, according to the positron emission tomography data, a diffuse decrease in the glucose metabolism rate (GMR_glu), significantly exceeding the extent of the zones of morphological/anatomical lesions, was present in the brain before treatment, while the minimal improvement was observed if the GMR_glu was sufficiently intact. These and other paradoxical results can be explained if the vegetative state is regarded as a stable pathological state of the brain, which offers new approaches to the treatment of this group of patients.     

Regeneration of photoreceptor organs in freshwater planarians at different levels of accumulation of natural methylmercury compounds

The effects of natural methylmercury compounds on regeneration of photoreceptor organs were studied in three freshwater planarians: Polycelis tenuis, Dugesia lugubris, and D. tigrina. Accumulation of methyl mercury in the planarian body suppressed regeneration of P. tenuis with numerous photoreceptor organs to a greater extent than in two other planarians that have only two eyes. High methyl mercury concentrations inhibited the restoration of photoreceptor organs in asexual and sexual D. tigrina races.