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Biomedical subjects

T T Berezov

Publications and source records attributed to T T Berezov.

At least 19 recordsLinked to original sources
PubMed2006

[Polyamines and mental diseases].

The authors make an attempt to understand and evaluate the role of polyamines in the development of endogenous mental diseases. The article is dedicated to distribution and exchange of polyamines in the central nervous system, their metabolic and regulatory associations with gamma-aminobutyric acid and dopaminergic systems, as well as to possible neuromediatory and neuromodulatory functions of polyamines. The paper is also concerned with effects of psychotropic agents on polyamine metabolism and contains a hypothesis on the role of polyamines in etiopathogenesis of schizophrenia.

Central Nervous System↗
PubMed2006

[Cholesterol is an important molecule in the processes of the synaptic plasticity and degeneration of neurons].

The importance of homeostasis of neural tissue to neuron functioning, the synaptic plasticity of the hippocampus, and laboratory animals' behavior was demonstrated by the authors earlier. A range of experimental data evidences that cholinergic neurotransmission, ionotropic and metabotropic receptors, excessive tau phosphorylation, alterations in amyloid-beta biochemistry, oxidative reactions, and other features of neurodegenerative processes depend on the precise regulation of cerebral cholesterol metabolism. Such results suggest that disturbances in cholesterol homeostasis are the common primary cause of the sporadic and familial forms of Alzheimer's disease, Down syndrome, Niemann-Pick disease type C, and explain the similarity of neurodegenerative signs in different degenerative diseases of the nervous system. The present work was introduced at an annual conference of American Society for Neuroscience, and is available as a scientific report at www.neurobiologyoflipids.org/content/3/7/.

Alzheimer Disease↗
PubMed2005

[The role of Alzheimer amyloid plaques in the mechanisms of neuron synaptic plasticity disturbance].

The authors studied hippocampal microscopic sections taken from transgenic mice expressing non-mutated human amyloid precursor protein (APP695), and age-matched non-transgenic control mice. The aim of the study was to reveal individual effects of plaque-like amyloid of aged (25.5 months) transgenic mice and diffuse amyloid of non-transgenic mice (verified by immunohistochemistry and Congo Red fluorescence) on synaptic plasticity. In vitro extracellular recording of excitatory postsynaptic potentials from hyppocampal CA1 area revealed impairment of input/output characteristics and long-term potentiation, and a several-millisecond delay of initial post-tetanic traces in aged transgenic vs. control mice. The results show that amyloid plaques (not diffuse amyloid) may be one of the causes of synaptic dysfunction in Alzheimer disease.

Alzheimer Disease↗
PubMed2005

[Mast cells of the mammary gland and of the regional lymph node in rats with breast cancer induced by N-methyl-N-nitrosourea].

Using the methods of light and electron microscopy, morphometric and functional characteristics of mast cell (MC) populations were studied in the mammary gland (MG) and regional lymph node (RLN) at different stages of breast cancer (BC) induced in 120 outbred female albino rats with the body mass of 120-150 g. BC was induced by subcutaneous injections of chemical cancerogen N-methyl-N-nitrosourea. MC numbers and activity in MG and RLN were found to increase at all stages of BC formation studied (64-180 days of cancerogen exposure). Gradual increase in MC degranulation rate and degree, MC disintegration closer to the center of the tumor, together with the appearance in the peritumorous tissues, in the tumor itself, and in RLN of numerous small, immature MC, by their morphometric parameters identical to the intestinal mucosal MC, may presumably indicate the decompensation phenomena in the system and of the approaching of process terminal stage.

Animals↗
PubMed2004

Kinetic characteristics of biochemical parameters during consupren therapy after allogenic transplantation of the kidney.

Changes in biochemical and common clinical parameters of the blood were detected in patients treated with consupren (cyclosporin) as the main immunosuppressant after allogenic transplantation of the kidney. Kinetic model for evaluation of treatment adequacy was based on therapeutic drug monitoring and monitoring of blood biochemistry in recipients of the primary kidney transplant. The k1, t1/2, C0, clearance (for hemoglobin), conditioned volume of distribution (for cyclosporin) of processes of biochemical parameters (toxicity markers) stabilization within the framework of a single-part kinetic model were determined.

Adolescent↗
PubMed2004

[Liposome-oriented transport of therapeutic drugs].

The attempts to use liposomes as containers for the transport of therapeutic drugs have been undertaken during the recent 40 years. However, the first success was achieved only in the 80-ies, when the sterically stabilized liposomes were invented. It was found that the liposome biological layer modified through, adding to it, certain polymers prolonged the blood circulation and reduced the capture of liposomes by RES cells. Elaboration of immunoliposomes, i.e. those conjugated with antibodies, was the next step in the path of perfecting the liposomes as a transport tool for the sake of binding with target-cells and to ensure the address-oriented delivery of drugs to a pathology focus. Preclinical and clinical testing of liposome-form of antitumor drugs witnessed to their lower toxicity and better pharmacokinetic indices; besides, they selectively accumulate themselves in tumor cells and have a more pronounced therapeutic effect even at lower doses of drugs in case of tumors resistant to the already made chemotherapy.

Animals↗
PubMed2003

Role of matrix metalloproteinases and their inhibitors in tumor invasion and metastasis.

The role of various matrix metalloproteinases (MMP)--such as gelatinases, stromelysins, matrilysin, collagenase-3, and membrane-bound MMP (MB-MMP)--in tumor invasion and metastasis is discussed. Data suggesting significance for malignant growth of the expression level of these enzymes and also of their activators and inhibitors are presented. It is concluded that at different stages of tumor progression the activity of different MMPs is displayed, which is regulated by various growth factors and oncogenes. Different malignancies are characterized by changes in activities of specific MMPs. Data are presented which show significance of the ratio between the MMP activity and that of tissue inhibitors of metalloproteinases (TIMP) in tumor invasion and metastasis, especially in connection with a dual role of TIMP as both MMP inhibitors and activators.

Humans↗
PubMed2003

[Cancer morbidity in the Republic of Northern Ossetia-Alania (1991-2000)].

The cancer morbidity in the Republic of North Ossetia-Alania is still high: 248.2 (1998), 243.1 (1999) and 241.3 (2000) per 100,000. The site distribution patterns varied significantly: the leading localizations in 1991 were trachea, lungs and bronchus--32.1; breast--28.3; skin--26.5; stomach--21.2 and hemopoietic organs--18.0. By the year 2000, the situation had changed dramatically: breast--60.2; skin--33.7 and respiratory system--20.4.

Breast Neoplasms↗
PubMed2002

L-Lysine alpha-oxidase: physicochemical and biological properties.

This review summarizes data on the properties of L-lysine alpha-oxidase, an enzyme that belongs to the group of oxidases of L-amino acids. This enzyme acts virtually only on L-lysine with a rather low Km yielding alpha-keto-epsilon-aminocaproic acid. The decrease in the level of the essential amino acid L-lysine and the formation of hydrogen peroxide during the reaction possibly provide the basis for the unique properties of L-lysine alpha-oxidase: cytotoxic, antitumor, antimetastatic, antiinvasive, antibacterial, and antiviral activities, as well as an immunomodulating effect. Native L-lysine alpha-oxidase and its immobilized forms are promising tools for determination of concentration of L-lysine in various biological materials.

Amino Acid Oxidoreductases↗
PubMed2002

[Morphological and biochemical features of cerebral beta-amyloidosis in long-livers].

This is the first assessment of the pathogenetic values of some environmental factors in the occurrence and progression of cerebral beta-amyloidosis (Alzheimer's disease, senile dementia) in long-livers of different climatic areas of the Republic of North Ossetia-Alania. New isoenzyme serum assays for determining creatine kinase BB-isoenzyme and the transaminase activity in the spinal fluid are proposed, which may be used as potential markers in the biochemical diagnosis of Alzheimer's disease. They can both provide valuable information on the severity of morphological lesions of cerebral cells in Alzheimer's disease and serve as the basis for the differential diagnosis of different forms of dementia wherein dystrophic changes in CNS cells are absent or slightly pronounced.

Aged↗
PubMed2001

The levels of soluble amyloid beta in different high density lipoprotein subfractions distinguish Alzheimer's and normal aging cerebrospinal fluid: implication for brain cholesterol pathology?

Several previous studies reported the association of the soluble form of amyloid beta (sA beta) protein, a major constituent of amyloid deposits in Alzheimer's disease (AD), with normal blood, cerebrospinal fluid (CSF) and central nervous system high density lipoproteins (HDLs). The present report aimed to elucidate the pattern of sA beta and apolipoprotein (apo) distribution in AD CSF-HDL subfractions. We studied AD CSF-HDL subfractions by SDS/PAGE and immunoblot analysis after CSF fractionation via density flotation ultracentrifugation. AD CSF was characterized by (i) increased sA beta and apo content of the HDL(1), and (ii) sA beta association with apoE and apoJ in HDL(2), HDL(3) and very high density lipoproteins. The finding supports our proposed hypothesis that upregulation of brain cholesterol dynamics is a fundamental event in the pathophysiology of AD and that sA beta binding to apo and lipid may have important structure-functional consequences.

Alzheimer Disease↗
PubMed2001

Matrix metalloproteinases of normal human tissues.

This review considers biochemical properties of the family of matrix metalloproteinases (MMPs) of normal human tissues and the involvement of these enzymes in morphogenesis. Four main MMP subfamilies are characterized, and a group of other MMPs is described. Data on mechanisms of activation and inhibition of MMPs in certain tissues during various physiological processes (embryogenesis, angiogenesis, tissue growth and involution) are considered. Information about tissue inhibitors of MMP is presented, and the ability of these inhibitors to regulate the activity of MMPs is analyzed.

Humans↗
PubMed2000

Role of matrix metalloproteinases in development of diabetic nephropathy.

This review considers molecular mechanisms that underlie disorders in the structure and metabolism of renal extracellular matrix in diabetic nephropathy. The contribution of the increased synthesis of renal extracellular matrix proteins in the accumulation of renal mesangial matrix is considered, and the important role of the degradation system of the extracellular matrix proteins in the development of fibrosis is also shown. Data on changes in mRNA expression for the matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) in various forms of diabetic nephropathy are presented. A correlation is established between changes in the balance of MMP proteolytic activity and TIMP activity and the accumulation of extracellular matrix.

Diabetic Nephropathies↗
PubMed1999

Beta-amyloid: Alzheimer's disease and brain beta-amyloidoses.

This review considers some aspects of the biochemistry of beta-amyloid, a protein which produces insoluble deposits in the brain. These deposits are a specific morphological feature of Alzheimer's disease, Down's syndrome, and senile dementia. Our contribution to the concept of a soluble form of beta-amyloid as of a normal human protein is presented.

Alzheimer Disease↗