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Biomedical subjects

N Popova

Publications and source records attributed to N Popova.

At least 19 recordsLinked to original sources
PubMed2005

Effects of TiO2, ZrO2 and Al2O3 dopants on the compressive strength of tricalcium phosphate.

Tricalcium phosphate (TCP) powders synthesised using the Ca(NO3)2 and Ca(OH)2 routes were doped with TiO2, ZrO2 and Al2O3 in order to increase their compressive strength. An ultimate compressive strength (UCS) of 255 +/- 6 MPa was achieved for approximately 10 vol% TiO2 doping compared to 30 +/- 3 MPa for an un-doped control processed and tested in the same manner. Higher levels of TiO2 doping resulted in smaller increases in UCS with 30 and 50 vol% achieving 213 +/- 9 and 178 +/- 15 MPa, respectively. Very small amounts of Al2O3 doping (< 0.5 vol%) also resulted in a stronger materials. However, under the processing conditions employed, higher levels of Al2O3 and ZrO2 doping resulted in no beneficial effect on the UCS. Polyvinyl alcohol (PVA) was used as binding agent to facilitate processing. As expected, higher levels of PVA were associated with smaller increases in UCS. Powders synthesised using the Ca(OH)2 route had smaller particle size and resulted in larger increases in UCS compared to the Ca(NO3)2-synthesised powders. Although some powders contained alpha and beta-TCP phases, no other calcium phosphate, CaO, CaTiO3 or CaZrO3 phases were detected. In conclusion, a significant increase in the UCS of TCP was achieved by doping with approximately 10 vol% TiO2 which is expected to have little or no effect on the bioactivity or bioresorbability of the material.

Aluminum Oxide↗
PubMed2000

A locus that influences susceptibility to 1, 2-dimethylhydrazine-induced colon tumors maps to the distal end of mouse chromosome 3.

While inheritance of mutated alleles of highly penetrant tumor suppressor genes such as retinoblastoma or p53 predisposes individuals to a greatly increased risk of developing cancer, epidemiological data indicate that the majority of sporadic tumors in humans result from interactions of environmental and host genetic factors. The host genetic factors are poorly penetrant tumor susceptibility genes that determine the likelihood that a cancer will arise from carcinogen exposure. The majority of colon tumors in humans are sporadic in nature. 1,2-dimethylhydrazine (DMH)-induced colon tumors in mice provide a useful animal model to identify genes that influence susceptibility to carcinogen-induced colon tumors in humans. A genome-wide scan of genetic crosses of relatively sensitive C57BL/6J with relatively resistant CBA mice treated with DMH revealed a linkage of DMH susceptibility with the distal end of mouse chromosome 3, suggesting that one or more tumor susceptibility genes may map to this region.

1,2-Dimethylhydrazine↗
PubMed1999

Congenital cataracts facial dysmorphism neuropathy syndrome, a novel complex genetic disease in Balkan Gypsies: clinical and electrophysiological observations.

During a study of hereditary motor and sensory neuropathy-Lom in Bulgaria, a previously unrecognized neurological disorder was encountered, mainly in Wallachian Gypsies, who represent a relatively recent genetic isolate. The disorder has been termed the congenital cataracts facial dysmorphism neuropathy (CCFDN) syndrome to emphasize its salient features. Fifty individuals from 19 extended pedigrees were identified and examined clinically and electrophysiologically. At least 1 patient from each family was admitted to the hospital in Sofia for full investigation. Pedigree analysis indicates autosomal recessive inheritance. The disorder is recognized in infancy by the presence of congenital cataracts and microcorneas. A predominantly motor neuropathy beginning in the lower limbs and later affecting the upper limbs develops during childhood and leads to severe disability by the third decade. Associated neurological features are a moderate nonprogressive cognitive deficit in most affected individuals together with pyramidal signs and mild chorea in some. Accompanying nonneurological features include short stature, characteristic facial dysmorphism, and hypogonadotrophic hypogonadism. Nerve conduction studies suggest a hypomyelinating/demyelinating neuropathy, confirmed by nerve biopsy. The CCFDN syndrome is thus a pleomorphic autosomal recessive disorder displaying a combination of neurological and nonneurological features.

Adolescent↗
PubMed1993

Immune responses in male mice with aggressive and submissive behavior patterns: strain differences.

Immune responses in two strains of male mice with aggressive and submissive behavior patterns was studied. In aggressive CBA males immunized on the 10th day of agonistic confrontations with submissive partners, greater numbers of plaque-forming cells (PFC) and rosette-forming cells (RFC) were noted compared to control mice. Unlike the CBA strain, both PFC and RFC levels in aggressive C57BL males did not increase, but both PFC and RFC numbers decreased in submissive animals.

Agonistic Behavior↗
PubMed1991

Regulation of the expression of the sex-specific isoforms of cytochrome P-450 in rat liver.

The hepatic metabolism of steroid hormones and of xenobiotics frequently depends on the expression of the sex-specific isoforms of cytochrome P-450 and on differences in sex hormones. Following biochemical, immunological and molecular biological investigations, it was shown that in adult rat liver there exist at least four male-specific and one female-specific isoforms of cytochrome P-450. The designation of these sex-specific genes is IIC11, IIIA2, IIC13 and IIA2 in males, and IIC12 in females. The irreversible programming of the expression of these isoforms of cytochrome P-450 in adulthood occurs during the perinatal period of life, and is named enzyme imprinting. One of the main factors that regulates the expression of the sex-specific isoforms of cytochrome P-450 is the level of androgens in the blood. Castration of adult rats decreased the level of the male isoforms of cytochrome P-450 and the activity of the monooxygenase enzyme system that remained higher than in intact females. The mechanism of enzyme imprinting can be explained as follows: neonatal androgens program the secretion of hypothalamic hormones, somatostatin and growth-hormone-releasing factor. These factors determine the type of growth hormone secretion in adult rats, and this controls the type of sex-specific isoforms of cytochrome P-450 expressed in adulthood. Metabolic regulation similar to that outlined above was shown to occur for several metabolism-dependent chemical carcinogens. Such a pathway may explain the different sensitivity displayed by male and female rats to treatment with these carcinogenic agents. One possible way of modulating the expression of some isoforms of cytochrome P-450 in adult rats is by treating neonates with specific xenobiotics that change the constitutive expression of neonatal androgens. It appears that this enzyme imprinting plays an important role in determining the individual sensitivity to the carcinogenic effects of chemicals.

Animals↗
PubMed1991

Changes in the enzyme activity of the myocardium and participation of the alpha-adrenergic and M-cholinergic systems in experimental isoprenaline myocardial hypertrophy.

With a view to clarifying the mechanisms of haemodynamic stress, as well as the role of some neurotransmitter systems in the pathogenesis of myocardial hypertrophy (MH), a complex of experiments was carried out with an MH model induced in rats by isoprenaline treatment and by applying the M-cholinolytic agent atropine and the alpha-adrenergic blocker phentolamine in a part of the experimental groups. The changes in the activity of some enzymes of myocardial metabolism, namely: glucose-6-phosphate dehydrogenase, pyruvate kinase, alpha-hydroxy-butyrate dehydrogenase, isocitrate dehydrogenase, malate dehydrogenase and creatine phosphokinase, were traced in 33 male Wistar rats. Considerable activation of glucose-6-phosphate dehydrogenase was found in the different experimental groups, suggesting the adaptive "anti-stress" character of this change. The results of the pathobiochemical studies presuppose the substantial participation of the alpha-adrenergic and of the M-cholinergic systems in the stage of compensated isoprenaline-induced myocardial hypertrophy.

Animals↗
PubMed1989

Comparative studies on catecholamine content and glycogen phosphorylase activity in the myocardium of spontaneously hypertensive and normotensive rats.

Myocardial noradrenaline (NA) and adrenaline (A) concentrations as well as phosphorylase (PHOS) activity in spontaneously hypertensive (SHR) and normotensive Wistar (NWR) rats 1.5, 3, 6, 12 and 18 months of age were assayed. Myocardial hypertrophy as determined by the heart/body weight ratio in 1.5 month old SHR preceded the onset of hypertension. The arterial blood pressure (ABP) of SHR was significantly elevated from month 3 onward attaining a maximum level at month 12. The concentrations of A and NA, and activity of PHOS "a" in SHR were lower than in NWR between months 3 and 12. The differences were marked in SHR 3 months of age, and corresponded to the ABP changes. An age-dependent decrease in A, NA and PHOS "a" in SHR was observed. The data suggest a role of catecholamines in the development of cardiac hypertrophy via regulation of metabolism.

Aging↗
PubMed1981

Content of prostaglandins E and F in the blood plasma and kidneys in arterial hypertension (clinical-experimental study).

A dynamic study is made of the content of PGE and PGF2 alpha in the kidneys of rats with experimental coarctation hypertension, as well as the PGF2 alpha-metabolite in the blood plasma of the same experimental model in rats and in patients with arterial hypertension. The level of the PGF2 alpha-metabolite tends to decrease both in the animals with experimental hypertension and in hypertonic patients. In rats with 30-day hypertension low values are established in 55 per cent, while in 45 per cent there are high values of the PGE level in the kidney homogenate compared with the control group. The concentration of PGF2 alpha in the left ("endocrine") kidney (whose artery originates distally from the place of aortic coarctation) is higher than the concentration of the same PG in the right kidney. Our findings give grounds for the following assumptions: 1. The PGF2 alpha-metabolite as hormone and partly PGE in the kidneys seem to be involved in the pathogenesis of arterial hypertension as compensatory factors. 2. PGF2 alpha in the kidneys probably participates directly as one of the elements of the complex pathogenesis of arterial hypertension.

Adolescent↗
PubMed1978

[Enzymatic activity in the uterine musculature of rats after castration and testosterone treatment].

The authors examined the activity of GOT, GPT, LDH and ALD in the myometrium of ovariectomized female rats, treated with testosterone. There was a eduction in the activity of the examined enzymes in both experimental groups of animals in comparison with the group of healthy rats. The reduction of the enzymic myometrial activity was considerably more manifested in the group of ovariectomized rats than in those treated with testosterone. The results were interpreted as a consequence of the reduced synthesis of proteins enzymes due to insufficient estrogen stimulation in the myometrial tissue, sensitive to estrogen. There was a possibility also that the reduction of the enzymic synthesis was caused by energetic deficit on account of insufficient transhydrogenase activity as a result of the reduced estrogen concentrations.

Alanine Transaminase↗