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Presented in the paper circuit enables automatic recording when the cytometer TsMK-I is used. The spectrum is recorded and displayed by means of the pulse analyzer Ae-128. The range of linear amplitude conversion of input pulses makes it possible to obtain the distribution bar chart with the class number no less than 100.
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Histochemical methods were used to assess the distribution of 4 neurotransmitters thought to be involved in cortical plasticity. They were measured in the primary auditory cortex of the ferret from just before the onset of hearing. Acetylcholinesterase staining was strongest in layers I, IV and VI and there was a gradual increase in the amount of staining from postnatal day (PND) 21 through to adulthood. Serotonin fibres were located mainly in layers I-III and their density increased gradually over the same time period. Noradrenergic fibres were sparsely scattered throughout the cortex but their density and distribution showed little change over the age range studied. Dopaminergic fibres were densest in layers V and VI at all ages. However, there was a transient doubling in their density that started round about the onset of hearing at PND 28, peaked at PND 35 and had returned to baseline levels by 2 wk later. This transient peak in density did not occur in the adjacent suprasylvian gyrus and did not appear to be a general phenomenon. The local transient increase in dopaminergic fibres implies that they may have an important role during a short period in auditory cortical development. This role may involve modifying the cortical circuitry that is involved in analysing the input from the auditory periphery.
The aim of the present study was to investigate the regulation of the apoAI gene by dietary saturated fat and cholesterol. Saturated fatty acids and cholesterol raise low density- and high density lipoprotein particles in humans. Increased LDL is attributed to the down-regulation of LDL-receptor gene, but the mechanism of increased plasma HDL levels is unknown. To study the mechanism of HDL elevation by saturated fat, male rats and male mice were employed as animal models, since they also raise their plasma HDL levels when fed high lipid diets. Animals were divided in four groups and fed the following diets: control (5% corn oil); high cholesterol (0.5%); high fat (20% coconut oil); and high fat plus cholesterol diets. The high cholesterol diet did not alter plasma and HDL-cholesterol levels. However, the high fat diet increased HDL levels by 20% in rats and 55% in mice. A combination of saturated fat and cholesterol diet raised plasma HDL levels by 36 and 67% in rats and mice, respectively. Plasma apoAI levels increased parallel to HDL concentrations. Mechanism of HDL elevation by saturated fat was investigated. Hepatic and intestinal apoAI mRNA did not change with any of the test diets in mice. Rat hepatic apoAI mRNA was also unchanged by the high cholesterol diet, but was decreased on high fat and fat-cholesterol combination diets. These results suggest that transcriptional regulation of the apoAI gene was not responsible for increased plasma apoAI and HDL. The translational efficiency of apoAI on isolated polysomes was also measured, and it was found that apoAI synthesis increased about 20% on high fat and fat-cholesterol combination diets. This partially explains the elevated levels of plasma HDL. Additional regulation through impaired catabolism of HDL particles by high fat diet feeding may be another pathway for increased HDL levels. Unlike apoAI mRNA, the mRNA of other HDL apoproteins, apoAII and apoAIV, were increased by high fat and combination diet feeding. These results suggest that saturated fatty acids regulate plasma HDL levels by translational and posttranslational mechanisms.
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The main clinical use of measurements of Apo Al and Apo B is to determine a patient's risk status for the development of ischemic heart disease. Apo B is generally accepted as a contributory cause of coronary artery disease, while Apo Al apparently has a protective effect. The present study reports the plasma change of Apo Al and B in sickle cell anaemic subjects. Immunochemical findings revealed that Apo Al and B levels were found to be lower in sickle cell patients as compared with normal subjects (HbAA). The atherogenicity index given by Apo B/Apo Al remained in the normal range during periods of steady state (0.64 +/- 0.28), while subjects in painful crisis had high index values (0.95 +/- 0.35). Therefore, we concluded that epidemiological studies on a large sample of patients are needed to confirm this relationship between painful crisis and risk of developing coronary artery disease.
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