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Biomedical subjects

M Iu Martynov

Publications and source records attributed to M Iu Martynov.

14 recordsLinked to original sources
PubMed2006

[Batroxobin in patients with ischemic stroke in the carotid system (the multicenter study)].

A randomized placebo-controlled study has been carried out in 3 Moscow hospitals. A sample included 90 patients who survived hemispheric ischemic stroke caused by pathology in the internal carotid artery 72 h before the treatment. Forty-five patients were given standard (basic) therapy and 45 patients received adjuvant batroxobin intravenously by 1,0 ml (10BU) drops on day 1, 3 and 5 and by 0,5 ml (5BU) drops on day 7 and 9 after admitting in a hospital. Assessment of the patients' state was conducted before the treatment, on day 3, 6 and 15. The European Stroke Scale was used to measure severity of clinical symptoms. The results suggest efficacy of batroxobin the use of which provides rapid good results, especially improvement in movement disorders. The use of this drug is accompanied by defibrinating effect. The drug is well tolerated.

Batroxobin↗
PubMed2005

[Thrombocyte-vascular and sero-coagulation hemostasis, and blood lipids in the acute period of ischemic stroke].

The subjects of the study were 46 patients at the acute stage of a first or repeated ischemic stroke (IS). The study revealed prevalence of procoagulating and thrombocyte activity of hemostasis, pronounced deficiency of physiological anticoagulants, high activity of Willebrand factor, and dislipidemia in these patients. The results show that secondary IS prophylaxy require combined antiaggregant therapy or combined therapy including anticoagulants and antithrombocyte agents plus correction of dislipidemia.

Acute Disease↗
PubMed2004

[Modeling of focal ischemia of the brain].

Methods of modeling and criteria of evaluating the pathological process in the central nervous system (CNS) as well as modern technologies of provoking the focal ischemia of the brain in experimental animals are under discussion. The results were analyzed comparatively from the viewpoint of efficiency and adequacy of certain models as well as of the clinical specificity of ischemic strikes in man and of set research goals. A literature analysis confirms that the existing arsenal of methodical schemes provides for choosing the most adequate model of focal ischemia of the brain and to ensure a cerebral infarction of a preset scope and localization; it makes possible also an objective evaluation of pathological processes occurring in the cerebral tissues both at the earliest stages of ischemic lesion and during a relatively long time period comparable with rehabilitation time period. Achievements in the sphere of experimental modeling of focal ischemia of the brain pave the way to further promotion of experimental therapy in acute stroke and open up new research priorities; it concerns primarily research of mechanisms timing the neurodegenerative process after ischemic stroke as well as searching-for and testing of means of stroke prevention and of patients' rehabilitation.

Animals↗
PubMed2004

[The we gene is a modifier of the wal gene in mice].

Interaction of gene wellhaarig (we) with genes waved alopecia (wal) and hairless (hr) was studied in mice. The mutant gene we is responsible for the development of a specific waved coat in homozygotes. Homozygous mice carrying mutant gene wal also have a wavy coat, though a partial alopecia develops with time in these animals. In homozygotes for the hr gene, hair loss is observed beginning from the age of ten days. A series of crosses we/we and wal/wal yielded animals with we/+wal/wal and we/we wal/wal genotypes. In mice we/+wal/wal carrying gene we at a single dose, alopecia is accelerated significantly as compared to the single-dose homozygotes +/+wal/wal. In we/we wal/wal mice, alopecia starts earlier than in we/+wal/wal mice; by the age of one month, the double homozygotes are almost hairless except for small body areas covered with a sparse coat. In addition, curliness of the first-generation hair in mice we/we wal/wal is much more expressed than in +/+wal/wal and we/we+/+ mice. The obtained evidence suggests that the we gene is a modifier of the wal gene because the former enhances the effects of the wal gene, which is confirmed by the earlier onset of alopecia and progression of the latter in mice having the we/+wal/wal genotype and especially in we/we wal/wal animals. The we/we hr/+ mice do not differ in coat from we/we+/+ mice; in both cases, the coat is wavy. The coat of double homozygotes we/we hr/hr, is similar to that of we/we+/+ mice until ten days of age, when the signs of alopecia appear. By the age of 21 days, mice we/we hr/hr have lost their coat completely like mice +/+ hr/hr. Hence, the we gene is a modifier of the wal gene though it does not interact with hr gene during the coat formation.

Animals↗
PubMed2004

[Markers of inflammation, autoantibodies to neurospecific antigens and outcome in patients with acute ischemic stroke].

To identify biochemical markers for carotid stroke outcome, blood serum levels of inflammation markers (C-reactive protein, orosomucoid, soluble p-selectin) and autoantibodies (AAB) to neurospecific antigens (glial fibrillary acidic protein, neuron specific enolase, S-100 protein) were studied in 27 patients (mean age 64 +/- 6 years) with acute ischemic stroke in inner carotid artery system on day 1-2 and 21 of the disease onset. To day 21, patients with good rehabilitation of neurological functions (group 1) demonstrated a decrease of C-reactive protein and soluble p-selectin concentrations, and unfavorable disease course was associated with a significant (p<0.05) increase of concentrations of these indices. On day 1 and 7, a level of AAT to glial fibrillary acidic protein was higher (p<0.05) in group 1 than in that with minimal rehabilitation and to day 21 it decreased relatively the baseline level. At the same time, patients with minimal rehabilitation had a stable AAT level. On day 7, the AAT level correlated with expression of neurological deficit on day 21 (r=0.510; p=0.019). No stroke-course-dependent differences were found in dynamics of orosomucoid as well as of AAT to neuron specific enolase and S-100 protein levels.

Acute Disease↗
PubMed2003

[Antihypertensive treatment with eprosartan mesilate of patients in acute and late periods of ischemic stroke].

Twenty patients with stroke of hemisphere localization developed as a result of arterial hypertension were treated with eprosartan mesilat. An estimation of the drug efficacy was conducted in comparison with other hypotensive medicines (control group). Eprosartan was used in dosage 600 mg daily. The study was carried out during 12 months, along with a monitoring of the most relevant hemodynamic indices, evaluation of somatic and neurological state of the patients as well as of some neuropsychological functions and quality of life, statistical significance of the results being determined. Pronounced hypotensive effect of the drug was found both in acute and late periods of stroke. Eprosartan mesilat monotherapy was effective in 75% of the patients. The most important feature proved to be a decrease of arterial pressure variability from the first days of the treatment, less frequency of secondary strokes being detected as well.

Acrylates↗
PubMed2002

[Eprosartan mesylate in controlling of blood pressure in patients with ischemic stroke].

In 20 patients with ischemic stroke and moderate or severe arterial hypertension the effectiveness of eprosartan mesilat (Teveten, Solway Farma, Germany) for a period of 6 months was studied. Patients received 600 mg of eprosartan mesilat daily and in 4 cases hydrochlortyaside was also added. Monotherapy with eprosartan mesilat was effective in all patients with moderate arterial hypertension and in 43.6% in patients with severe arterial hypertension. Therapy with eprosartan mesilat was associated with significant hypotensive effect (more evident in patients with high systolic blood pressure), improvement in 24-hour blood pressure profile and quality of life, and lower probability of secondary stroke. Side effects were not observed.

Aged↗
PubMed2001

[Surgical treatment of asymptomatic carotid arteries stenosis].

Vascular diseases of the brain is one of the major causes of disability and mortality in the developed countries and particular attention is devoted to their prevention. Current approaches to carotid endarterectomy as one of the ways of prevention of transient ischemic attacks and ischemic strokes are presented in this review. The results of major multicenter studies, peri- and postoperative complications and high-risk groups for the development of ischemic stroke are analyzed.

Carotid Stenosis↗
PubMed1997

[Magnetic resonance angiography in patients with ischemic vertebrobasilar stroke].

The analysis of sensitivity and specificity of magnetic resonance angiography (MRA) was performed in investigation of vertebral and basilar arteries in 29 patients with acute vertebrobasilar insufficiency. MRA data were compared with the results of ultrasonic dopplerography of the same vessels including duplex scanning and figures subtractive angiography. Highly satisfactory efficiency of MRA was demonstrated. Peculiarities of both visualization of the intact vessels and of different variations of their obstruction as well as indications for performing diagnostic MRA are considered.

Adult↗
PubMed1991

[A clinico-neurophysiological analysis and the treatment problems of the crush syndrome (based on data from the earthquake in Armenia)].

Overall 350 patients with the crush syndrome were examined. It has been shown by the clinico-neurological investigation that in long compression of the limbs followed by the development of the crush syndrome, sensitive fibers and the membrane of the axon are most of all exposed to unfavourable effects. The changes discovered as a result of the clinically intact nerves point to the diffuse impairment of the peripheral neuromotor apparatus in patients with the crush syndrome.

Armenia↗