PubMed Health⌕ Search

Biomedical subjects

K M Lakin

Publications and source records attributed to K M Lakin.

At least 19 recordsLinked to original sources
PubMed2001

1/f frequency noise of 2-GHZ high-Q thin-film sapphire resonators.

We present experimental results on intrinsic 1/f frequency modulation (FM) noise in high-overtone thin-film sapphire resonators that operate at 2 GHz. The resonators exhibit several high-Q resonant modes approximately 100 kHz apart, which repeat every 13 MHz. A loaded Q of approximately 20,000 was estimated from the phase response. The results show that the FM noise of the resonators varied between Sy (10 Hz) = -202 dB relative (rel) to 1/Hz and -210 dB rel to 1/Hz. The equivalent phase modulation (PM) noise of an oscillator using these resonators (assuming a noiseless amplifier) would range from [symbol: see text](10 Hz) = -39 to -47 dBc/Hz.

Journal Article↗
PubMed1990

[Hemostatic potential during the development of post-mastectomy edema].

The work deals with the study of the mosaic character of the hemostatic potential, connected with the development of a localized pathological process, taking postmastectomy edema in illustration. It is shown that this condition is an example of the manifestation of the RASK system mosaics in one organism in pathology. It should be pointed out that the degree of the development of the local DVS syndrome changes significantly some of the RASK system parameters at the level of the whole organism. This is evidence that normalization of the microcirculatory processes in the edematous extremity will be an important measure in complex treatment of postmastectomy edema. It will considerably lower the risk of general disorders of the RASK system. Parameters determined in the blood collected from the extremity on the side of the operation will serve as controls of the efficacy of the applied therapeutic measures.

Arm↗
PubMed1990

[Changes in the level of polyunsaturated fatty acids, substrates and inhibitors of thromboxane and prostacyclin synthesis, in the blood of patients with cardiovascular diseases].

The authors examined the ratios of blood free polyunsaturated fatty acids (PUFA), such as 20:3n6, 20:4n6, 20:5n3, and 22:6n3, which are substrates and inhibitors of synthesis of thromboxane A2 and prostacyclins that regulate both normal blood fluidity, and platelet adhesion and primary thrombogenesis. The object of the study was plasma from healthy subjects and 4 groups of patients with cardiovascular diseases: 1) large myocardial infarction; 2) resting and exercise-induced angina pectoris; 3) large myocardial infarction; and 4) recurrent myocardial infarction. The levels of plasma free PUFA were measured by gas chromatography. Assessment of the PUFA ratios indicated that the risk for thrombogenesis increased in large and recurrent myocardial infarctions as compared to small myocardial infarction and angina pectoris both by reducing the relative levels of 20:3n6 and, in particular, 20:5n3, substrates of synthesis of only thrombolytics and vasodilators and by more greatly inhibiting the synthesis of prostacyclins than thromboxane with elevated 22:6n3 levels.

Aged↗
PubMed1986

[Action of nonsteroidal anti-inflammatory agents on fibrinolysis and platelet aggregation].

The influence of non-steroidal antiphlogistics (NSA, fluor derivatives of phenylanthranilic acid) on fibrinolysis, platelet function, prostaglandin metabolism and pharmacokinetics of indirect anticoagulants was studied in rats and rabbits in vitro and in vivo. NSA were found to shorten the euglobulin lysis time and to enlarge the lysis zones on fibrin plates. They potentiated the fibrinolytic activity of streptokinase and trypsin. Furthermore, they inhibited platelet aggregation induced by arachidonic acid in rabbits. NSA in combination with inhibitors of thromboxane synthetase potentiated inhibition of aggregation. After oral administration, NSA inhibited formation of thromboxane A2 and prostacyclin in rabbits in a dose-dependent manner. At comparatively low doses, thromboxane A2 synthesis was more effectively inhibited than prostacyclin formation. Due to pharmacokinetic interactions NSA enhanced the anticoagulant effect of indirect anticoagulants and accelerated their distribution and elimination.

Animals↗
PubMed1985

Influence of cholesterol and prostaglandin E1 on the molecular organization of phospholipids in the erythrocyte membrane. A fluorescent polarization study with lipid-specific probes.

Anthryl-labeled fluorescent probes closely mimicking phosphatidylcholine and sphingomyelin were applied to study the state of these phospholipids in the rabbit erythrocyte membrane. At normal cholesterol levels both probes exhibited higher fluorescence polarization values in the membranes than in phospholipid vesicles of similar lipid composition, indicating a decreased fluidity of the probe environment in erythrocyte ghosts. In ghosts prepared from normal erythrocytes no evidence of lateral separation of phosphatidylcholine and sphingomyelin was found. At higher cholesterol levels, however, these lipids appear to segregate. Probably the effect of cholesterol on the erythrocyte membrane lipids involves lipid-protein interactions. At physiological concentrations, prostaglandin E1 only weakly affects the state of phosphatidylcholine and sphingomyelin in erythrocyte membranes. Cholesterol enrichment amplifies the effect of prostaglandin E1. Although the prostaglandin E1-induced changes depended much upon whether the ghosts were enriched with cholesterol in vitro or in vivo, with both types of ghosts effects of prostaglandin E1 were seen at extremely low effector concentrations that may have presented a few molecules of prostaglandin per ghost. The structural and functional significance of these findings is discussed.

Alprostadil↗
PubMed1979

[Study of the effect of various intermediate products and enzymes of carbohydrate metabolism on erythrocyte aggregation].

The effect of some substances on the aggregation of red blood cells induced by gamma-globulin and fibrinogen was studied in vitro. Fructose 1,6-diphosphate, glucose 6-phosphate, glyceraldehyde dehydrogenase, insulin and prostaglandin E1 inhibited aggregation of red cells. Glucose, glucose 1,6-phosphate and ACTH had different effects in various concentrations on red cell aggregation, while fructose, prednisolon and D-oxy-prostaglandin E1 alpha and E1 beta caused no effect.

Adrenocorticotropic Hormone↗
PubMed1979

[Effect of aggregation inducers and inhibitors on the functional properties and the ultrastructure of platelets].

The influence of inductors and inhibitors of platelet aggregation on certain functional properties and structural peculiarities of platelets are investigated. Inductors of aggregation, such as ADP and thrombin, will cause the calcium binding to the platelet membrane to be diminished, whereas inhibitory substances of platelet aggregation will cause an increase of calcium binding. Inductors increase the number of partially degranulated platelets. Inhibitors, such as triphtazin and papaverin, inhibit these morphological changes.

Adenosine Diphosphate↗