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Biomedical subjects

A V Medvedev

Publications and source records attributed to A V Medvedev.

At least 19 recordsLinked to original sources
PubMed2003

Polarization splitting of optical resonant modes in a-Si:H/a-SiO(x):H microcavities.

We present experimental and theoretical results on polarization splitting of optical resonant modes in a-Si:H/a-SiO(x):H microcavities. It is shown experimentally that the splitting sign and value can be controlled by varying the active layer thickness. The polarization splitting achieved in the microcavities is about 8 meV owing to a large optical contrast, which is the ratio of film refractive indices in the distributed Bragg reflectors. The experimental data and theoretical analysis show that the polarization splitting may be zero at a certain angle of incidence of light determined by the microcavity parameters. The measured and calculated resonant frequency values for TM and TE polarizations were used to find the optical thickness of the active layer and the stop-band center frequency of the Bragg reflector. The account of the active layer thickness fluctuations along the lateral direction provides a better fit between the experimental and theoretical spectra.

Journal Article↗
PubMed2003

Persistent abnormality detected in the non-ictal electroencephalogram in primary generalised epilepsy.

OBJECTIVES: Gamma oscillations (30-100 Hz gamma electroencephalographic (EEG) activity) correlate with high frequency synchronous rhythmic bursting in assemblies of cerebral neurons participating in aspects of consciousness. Previous studies in a kainic acid animal model of epilepsy revealed increased intensity of gamma rhythms in background EEG preceding epileptiform discharges, leading the authors to test for intensified gamma EEG in humans with epilepsy. METHODS: 64 channel cortical EEG were recorded from 10 people with primary generalised epilepsy, 11 with partial epilepsy, and 20 controls during a quiescent mental state. Using standard methods of EEG analysis the strength of EEG rhythms (fast Fourier transformation) was quantified and the strengths of rhythms in the patient groups compared with with controls by unpaired t test at 1 Hz intervals from 1 Hz to 100 Hz. RESULTS: In patients with generalised epilepsy, there was a threefold to sevenfold increase in power of gamma EEG between 30 Hz and 100 Hz (p<0.01). Analysis of three unmedicated patients with primary generalised epilepsies revealed an additional 10-fold narrow band increase of power around 35 Hz-40 Hz (p<0.0001). There were no corresponding changes in patients with partial epilepsy. CONCLUSIONS: Increased gamma EEG is probably a marker of the underlying ion channel or neurotransmitter receptor dysfunction in primary generalised epilepsies and may also be a pathophysiological prerequisite for the development of seizures. The finding provides a new diagnostic approach and also links the pathophysiology of generalised epilepsies to emerging concepts of neuronal correlates of consciousness.

Adult↗
PubMed2001

beta-Adrenergic activation of p38 MAP kinase in adipocytes: cAMP induction of the uncoupling protein 1 (UCP1) gene requires p38 MAP kinase.

Because of increasing evidence that G protein-coupled receptors activate multiple signaling pathways, it becomes important to determine the coordination of these pathways and their physiological significance. Here we show that the beta(3)-adrenergic receptor (beta(3)AR) stimulates p38 mitogen-activated protein kinase (p38 MAPK) via PKA in adipocytes and that cAMP-dependent transcription of the mitochondrial uncoupling protein 1 (UCP1) promoter by beta(3)AR requires p38 MAPK. The selective beta(3)AR agonist CL316,243 (CL) stimulates phosphorylation of MAP kinase kinase 3/6 and p38 MAPK in a time- and dose-dependent manner in both white and brown adipocytes. Isoproterenol and forskolin mimicked the effect of CL on p38 MAPK. In all cases activation was blocked by the specific p38 MAPK inhibitor SB202190 (SB; 1-10 microm). The involvement of PKA in beta(3)AR-dependent p38 MAPK activation was confirmed by the ability of the PKA inhibitors H89 (20 microm) and (R(p))-cAMP-S (1 mm) to block phosphorylation of p38 MAPK. Treatment of primary brown adipocytes with CL or forskolin induced the expression of UCP1 mRNA levels (6.8- +/- 0.8-fold), and this response was eliminated by PKA inhibitors and SB202190. A similar stimulation of a 3.7-kilobase UCP1 promoter by CL and forskolin was also completely inhibited by PKA inhibitors and SB202190, indicating that these effects on UCP1 expression are transcriptional. Moreover, the PKA-dependent transactivation of the UCP1 promoter, as well as its sensitivity to SB202190, was fully reproduced by a 220-nucleotide enhancer element from the UCP1 gene. We similarly observed that increased phosphorylation of ATF-2 by CL was sensitive to both H89 and SB202190, while phosphorylation of cAMP-response element-binding protein was inhibited only by H89. Together, these studies illustrate that p38 MAPK is an important downstream target of the beta-adrenergic/cAMP/PKA signaling pathway in adipocytes, and one of the functional consequences of this cascade is stimulation of UCP1 gene expression in brown adipocytes.

Adipocytes↗
PubMed2001

Transcriptional regulation of the mouse uncoupling protein-2 gene. Double E-box motif is required for peroxisome proliferator-activated receptor-gamma-dependent activation.

Uncoupling protein-2 (UCP2) is present in many tissues with relevance to fuel metabolism, and its expression is increased in fat and muscle in response to elevated circulating free fatty acids resulting from fasting and high fat feeding. We proposed a role for peroxisome proliferator-activated receptor-gamma (PPARgamma) as a mediator of these physiological changes in UCP2, because thiazolidinediones also increase expression of UCP2 in these cell types (). To determine the molecular basis for this regulation, we isolated the 7.3-kilobase promoter region of the mouse UCP2 gene. The -7.3-kilobase/+12-base pair fragment activates transcription of a reporter gene by 50-100-fold. Deletion and point mutation analysis, coupled with gel shift assays, indicate the presence of a 43-base pair enhancer (-86/-44) that is responsible for the majority of both basal and PPARgamma-dependent transcriptional activity. The distal (-86/-76) part of the enhancer specifically binds Sp1, Sp2, and Sp3 and is indistinguishable from a consensus Sp1 element in competition experiments. Point mutation in this sequence reduces basal activity by 75%. A second region (-74/-66) is identical to the sterol response element consensus and specifically binds ADD1/SREBP1. However, deletion of this sequence does not affect basal transcriptional activity or the response to PPARgamma. The proximal portion of the enhancer contains a direct repeat of two E-Box motifs, which contributes most strongly to basal and PPARgamma-dependent transcription of the UCP2 promoter. Deletion of this region results in a 10-20-fold reduction of transcriptional activity and complete loss of PPARgamma responsiveness. Point mutations in either E-Box, but not in the spacer region between them, eliminate the stimulatory response to PPARgamma. However, gel shift assays show that PPARgamma does not bind to this region. Taken together, these data indicate that PPARgamma activates the UCP2 gene indirectly by altering the activity or expression of other transcription factors that bind to the UCP2 promoter.

Animals↗
PubMed2001

Temporal binding at gamma frequencies in the brain: paving the way to epilepsy?

Fast (beta-gamma band 20-100 Hz) rhythms of electrical activity of the brain have been suggested to play an important role in perception, cognition and consciousness providing temporal binding of neural activities and allowing the formation of mental representations. The recent advances in the concept of temporal binding and their relation to the theory of neural networks (connectionism) are reviewed here as well as some experimental results concerning the intensified gamma rhythms and epilepsy. The hippocampal-neocortical gamma rhythms are extremely intense and hypersynchronous at onset of the epileptiform discharges induced by systemic kainic acid in the rat. Those gamma rhythms are followed by a slow rhythm of epileptiform spikes/sharp waves or spike-wave complexes ('spike-wave' activity). During spike-wave activity, gamma synchronisation is significantly decreased. A novel unifying concept is proposed which relates the associative principle of neural networks to the mechanism of temporal binding at high frequencies. It suggests that for each memory stored in an associative network there is a corresponding quasi-stable state of synchronous oscillation at some frequency within the gamma band. It also suggests that excessive temporal binding ("over-binding") occurs at seizure onset when abnormally intensified and globally synchronous fast activity is often observed. "Over-binding" may cause the undesirable formation of false associations due to inadequate synaptic modifications. To prevent this process, spike-wave discharge develops as an extreme activation of the mechanism capable to desynchronise and eventually suppress fast activity and erase the spurious modes of activity associated with hypersynchronous gamma rhythms. Thus, spike-wave activity is suggested to be the "anti-binding" mechanism. This mechanism is also related to the spikes/sharp waves normally occurring in the brain mostly in sleep. It is qualitatively similar to the "unlearning" mechanism of Crick and Mitchison presumably associated with the PGO spikes of the REM sleep.

Action Potentials↗
PubMed2001

Adrenoceptors, uncoupling proteins, and energy expenditure.

Interest in the biology of adipose tissue has undergone a revival in recent years with the discovery of a host of genes that contribute to the regulation of satiety and metabolic rate. The catecholamines have long been known to be key modulators of adipose tissue lipolysis and the hydrolysis of triglyceride energy stores. However, more recent efforts to understand the role of individual adrenergic receptor subtypes expressed in adipocytes and their signal transduction pathways have revealed a complexity not previously appreciated. Combined with this interest in the modulation of adipocyte metabolism is a renewed focus upon brown adipose tissue and the mechanisms of whole body thermogenesis in general. The discovery of novel homologs of the brown fat uncoupling protein (UCP) such as UCP2 and UCP3 has provoked intensive study of these mitochondrial proteins and the role that they play in fuel metabolism. The story of the novel UCPs has proven to be intriguing and still incompletely understood. Here, we review the status of adipose tissue from inert storage depot to endocrine organ, interesting signal transduction pathways triggered by beta-adrenergic receptors in adipocytes, the potential of these receptors for discriminating and coordinated metabolic regulation, and current views on the role of UCP2 and UCP3 based on physiological studies and gene knockout models.

Adipocytes↗
PubMed2000

Direct binding of activated c-Src to the beta 3-adrenergic receptor is required for MAP kinase activation.

Both beta(2)- and beta(3)-adrenergic receptors (ARs) are able to activate the extracellular signal-regulated kinase (ERK) pathway. We previously showed that c-Src is required for ERK activation by beta(2)AR and that it is recruited to activated beta(2)AR through binding of the Src homology 3 (SH3) domain to proline-rich regions of the adapter protein beta-arrestin1. Despite the absence of sites for phosphorylation and beta-arrestin binding, ERK activation by beta(3)AR still requires c-Src. Agonist activation of beta(2)AR, but not beta(3)AR, led to redistribution of green fluorescent protein-tagged beta-arrestin to the plasma membrane. In beta-arrestin-deficient COS-7 cells, beta-agonist-dependent co-precipitation of c-Src with the beta(2)AR required exogenous beta-arrestin, but activated beta(3)AR co-precipitated c-Src in the absence or presence of beta-arrestin. ERK activation and Src co-precipitation with beta(3)AR also occurred in adipocytes in an agonist-dependent and pertussis toxin-sensitive manner. Protein interaction studies show that the beta(3)AR interacts directly with the SH3 domain of Src through proline-rich motifs (PXXP) in the third intracellular loop and the carboxyl terminus. ERK activation and Src co-precipitation were abolished in cells expressing point mutations in these PXXP motifs. Together, these data describe a novel mechanism of ERK activation by a G protein-coupled receptor in which the intracellular domains directly recruit c-Src.

Adipocytes↗
PubMed2000

[The use of clopixole in therapy of aged mental patients].

On the base of clinical psychological and electrophysiological studies of 34 patients with primary manifestations of brain circulation insufficiency good tolerance and high efficiency of Tanakan course treatment (3 x 40 mg/day for 3 months) were showen. Tanakan decreased manifestations of clinical syndrome, improved psychological functions and electrophysiological parameters. Prospective study supported the stability of positive changes in the status of patients for 12 months after Tanakan course treatment.

Aged↗
PubMed2000

[The aged patient's first visit to the outpatient psychiatric clinic].

160 patients over 60 years of age appealed to gerontologic unit of out-patient psychiatric clinic for the first time. The patients were divided into two main groups: with organic mental disorders (OMD) and with functional mental disorders (FMD) (79 and 81 patients, respectively). In the group of OMD the main form of disturbances were cases with dementia (74.4%) mainly of the Alzheimer's type, and cerebral vascular dementia. In 25.3% of the patients the cognitive disturbances didn't attain the level of dementia. In a group of patients with different forms of dementia a high frequency of comorbid mental pathology was observed (83%)--confusional states, delusions, depressive conditions as well as disturbed behavior (67.7%) that was one of the reasons for consulting a psychiatrist. In FMD group the prevailing pathology were depressions, both of the major (37.1%) and mild (34.6%) forms. The remaining cases were characterized by delusions (10.1%), anxiety-phobic (7.6%) states and somatoform disturbances (5.1%). Among the patients both of OMD and FMD groups it was possible to diagnose approximately 3-4 different somatic diseases; vascular and gastrointestinal disorders were met more frequently. The study of contribution of brain computer tomography (CT) to diagnosis of mental pathology (according to ICD-10), has demonstrated that in 30.8% of the cases it was decisive, in 41% it confirmed the clinical data and in 21.8% CT provide additional data (detecting latent cerebral vascular damage). And only in 6.4% of the cases CT fails to give definite information in diagnostically complicated cases. In 26.6% of the patients with FMD, CT of brain had detected symptoms of mild vascular pathology.

Aged↗
PubMed1999

E1A + cHa-ras transformed rat embryo fibroblast cells are characterized by high and constitutive DNA binding activities of AP-1 dimers with significantly altered composition.

Transcription factors of the AP-1/ATF family, including c-Fos, c-Jun, and ATF-2, play an important role in the regulation of cell proliferation and differentiation, and changes in their levels and/or activities may contribute to oncogenesis. We analyzed the alterations of AP-1/ATF transcription factors upon immortalization and transformation in a panel of cell lines derived from rat embryo fibroblast (REF) cells. The tumorigenic E1A + cHa-ras cells are characterized by high and constitutive DNA binding activities of AP-1, in contrast to nontransformed cells and the E1A cells. The expression of c-fos and c-jun genes was affected differently by the oncogenic transformation. By using antibodies to c-Jun and c-Fos proteins in electrophoretic mobility shift assays (EMSA), we showed that E1A + cHa-ras transformants did not contain c-Fos under any condition of cell cultivation and growth factor stimulation, whereas c-Jun was constitutively upregulated. In the absence of c-fos gene expression, c-Fos protein appears to be replaced by proteins of Fos family (Fra-1) and ATF family (ATF-2 and ATFa). To determine the possible mechanisms of c-fos downregulation in E1A + cHa-ras transformants we have obtained populations of geneticin-resistant clones containing integrated reporter construct -711fos-CAT and its mutants in serum-responsive element (SRE) and cAMP-responsive element (CRE). Data obtained show that the mutations within the SRE lead to a manifold activation of fos-CAT expression. This allows to suggest that c-fos downregulation in E1A + cHa-ras transformants is provided by a negative control mediated through the SRE regulatory region. The profound differences in regulation and composition of transcription factors of the AP-1 family probably play a pivotal role in the transformation of REF cells by E1A and cHa-ras oncogenes.

Adenovirus E1A Proteins↗
PubMed1997

[Use of cerebrolysin in the treatment of prolonged extrapyramidal complications of neuroleptic therapy].

Open study was performed concerning the efficiency of cerebrolysin in treatment of tardive dyskinesia and parkinsonism. 30 patients of middle (18-41 years) and old (60-82 years) age were examined by means of Extrapyramidal Symptom Rating Scale and Abnormal Involuntary Movement Scale. Cerebrolysin was administered intravenously by drops every other day in a dose of 5-10 ml during 28 days. Significant decrease of the severity of extrapyramidal symptoms (according to the Scales used) was observed by the end of the course of therapy. The number of the responders was 46.6%, of the partial responders--26.6%. Efficiency of cerebrolysin was the same both in the groups of patients with drug-induced parkinsonism (number of the responders--54.5%) and in patients with tardive dyskinesia (the responders' number--60%). The efficiency of cerebrolysin was lower in patients with combination of symptoms of parkinsonism and tardive dyskinesia as well as in ones with pronounced negative schizophrenic disorders in clinical picture. Efficacy of cerebrolysin was also the same in patients of both middle and old age. Its efficiency was equally high independently on the duration of extrapyramidal disorders' existence.

Adolescent↗
PubMed1995

[The characteristics of the cognitive defect in patients with different variants of late paranoia].

Evoked cortical activity in response to acoustic stimuli (oddball paradigm) was studied in patients with different paranoid disorders. The analysis covered the N150 negative wave and positive complex P300. In patients with paranoid schizophrenia and paranoid form of involutional psychosis cortical responses to the stimuli and cortex effects were not recorded. Such cognitive deficiency is believed to be typical for schizophrenia.

Aged↗
PubMed1993

[Retinoic acid intensifies the suppression of the proliferation of K562 cells by phorbol ester].

The effect of forbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) on the growth of cultured human chronic promyelocytic leukemia (K562) cells has been studied using cells growing in a medium consisting of RPMI 1640 supplemented with 10% fetal serum and with or without retinoic acid. All the used concentrations of TPA (100.0, 10.0, 1.0 and 0.1 ng/ml) cause the expected inhibition of proliferation of these cells. Moreover, a block of proliferation of K562 cells became stronger after cotreatment with TPA and retinoic acid, although this acid itself did not have any effect on proliferation and differentiation of K562 cells.

Cell Division↗
PubMed1992

Clinico-tomographical aspects in the pathogenesis of vascular dementia.

This article discusses the role of some pathogenetical factors in the main morphological variants of vascular dementia and their correlation with certain clinical parameters. On the basis of computer-tomographical (CT) studies of 62 patients with dementia, it was possible to distinguish three groups of patients, according to the type of parenchymatous brain lesions: (1) 14 patients with "pure" leukoaraiosis (LA); (2) 23 patients with ischemic foci (IF), and (3) 25 patients with a combination of LA and IF. A comparative study of these groups confirmed the concept that in the development of LA and dementia related to it, a special role is being attributed to such factors as arterial hypertension and aging.

Aged↗
PubMed1992

[Computerized tomography approaches in the study of dementia].

Computed tomography was used to study the prevalence rates of various types of intracranial pathology, hydrocephalus (HDC) and cortical atrophy (CA) in patients with late dementia (LD) and to comparatively assess the informative value of tomographic methods of cerebral morphometry. Computed tomographic data were obtained from 432 patients with LD. Despite the type of dementia, the authors revealed intracranial abnormalities of various etiology in 24.5%, postischemic foci being prevalent. Tumors, arachnoidal cysts, and chronic subdural hematomas were more infrequently diagnosed (in 2.6% of cases). HDC and CA were detected in 81.5 and 82.2% of patients with LD, respectively.

Aged↗
PubMed1992

[Ultrasonic scanning and duodenoscopy in the diagnosis and treatment of obstructive jaundice].

In 186 patients with obstructive jaundice admitted to the clinic for diagnosis of its cause, the ultrasound scanning with duodenoscopy was employed. This permitted to establish the cause of jaundice in 84.9% of the patients and to choose proper therapeutic tactics at the shortest time after hospitalization. In 80% of the patients, an obstacle for bile outflow was liquidated by means of endoscopy. When it was not possible to established the cause of jaundice by the findings of ultrasound scanning and duodenoscopy, percutaneous transhepatic cholangiography was performed, which has proved to be successful in 5.9% of cases. Use of the given methods for diagnosis permitted to define the optimal therapeutic tactics in patients with obstructive jaundice, to reduce the lethality.

Acute Disease↗