Relationship between postabsorptive respiratory exchange ratio and plasma free fatty acid concentrations

The relationship between overnight postabsorptive (fasting) respiratory exchange ratio (RER) and plasma FFA concentrations was addressed using data from three separate protocols, each of which involved careful control of the antecedent diet. Protocol 1 examined the relationship between fasting RER and the previous daytime RER. In Protocol 2 fasting, RER and plasma palmitate concentrations were measured in 29 women and 31 men (body mass index <30 kg·m⁻²). Protocol 3 analyzed data from Nielsen et al. (Nielsen, S., Z. K. Guo, J. B. Albu, S. Klein, P. C. O''Brien, M. D. Jensen. 2003. Energy expenditure, sex and endogenous fuel availability in humans. J. Clin. Invest. 111: 981-988.) to understand how fasting RER and palmitate concentrations relate within individuals during four consecutive measurements. The results were as follows: 1) Fasting RER was correlated (r = 0.74, P < 0.001) with the previous day''s average RER, and less so with RER variability. 2) Fasting RER was correlated (r = −0.39, P = 0.007) with fasting plasma palmitate concentrations. 3) The pattern of the RER/palmitate relationship was similar within individuals and between individuals; a negative slope was observed significantly more often than a positive slope (χ² test; P < 0.001). Our findings suggest that, despite a fixed food quotient, the slight departures from energy equilibrium in a controlled General Clinical Research Center environment can effect plasma FFA concentrations. We suggest that including indirect calorimetry as part of FFA metabolism studies may aid in data interpretation.     

Effect of precursors on biosynthesis of monensins A and B

Precursors of monensins (acetate, propionate, butyrate, isobutyrate) affect the total production and the relative proportion of monensins A and B. Addition of propionate into the fermentation medium causes a prevalence of monensin B whereas butyrate and isobutyrate stimulate the production of monensin A and suppress the production of monensin B.     

Modulating effect of cerulein on benzodiazepine receptors

Subcutaneous administration of caerulein (100-500 micrograms/kg) significantly reduced the development of picrotoxin (8 mg/kg) seizures in male mice. The same doses of caerulein inhibited 3H-flunitrazepam binding in in vivo experiments. Proglumide, an antagonist of cholecystokinin receptors, in low dose (5 mg/kg) potentiated the effects of caerulein (100 micrograms/kg), whereas the administration of proglumide in high dose (25 mg/kg) reduced the action of caerulein on 3H-flunitrazepam binding and picrotoxin seizures. Caerulein (5-1000 nM) decreased 3H-flunitrazepam binding in in vitro experiments only after supplementation of the binding medium with 120 mM NaCl and 5mM KCl. The results suggest the possible interaction of caerulein with chloride ionophor. It seems probable that the direct interaction of caerulein with chloride ionophor in involved in the inhibitory effect of caerulein on picrotoxin seizures and 3H-flunitrazepam binding.     

Analogs of oxytocin containing a modified peptide bond

Analogs of deamino-oxytocin and deamino-oxypressin containing a CH2-NH group instead of an amide bond between positions 8 and 9 were synthesized. All tested compounds exhibit significantly lowered biological activities.     

Purification and properties of thyrotrophin releasing hormone (TRH)-containing particles from the rat hypothalamus

The subcellular distribution of the TRH-like immunoreactivity in the rat hypothalamus and brain was studied. In differential centrifugation, the 900 g for 10 min supernatant (S1) of the hypothalamus or brain contained 61--79% of the total TRH. At 11,000 g for 20 min, 51--73% of the TRH in S1 was sedimented. When the hypothalamic S1 was fractioned under non-equilibrium conditions at 25 degrees C, two populations of TRH-containing particles were observed in several types of continuous linear density gradients. Metrizamide and sucrose gradients affected TRH-assay. TRH-particles were very light in Percol-gradients. Isotonic dextran 40,000-sucrose gradients gave the most reproducible results. In these gradients, the large TRH-particles (35%) equilibrated at 1.055--1.060 kg/l and the small ones (23%) at 1.041--1.047 kg/l. Working at 4 degrees C decreased the amount of large TRH-particles. The apparently larger particles contained cytoplasmic and mitochondrial enzymes and were sensitive to hypoosmotic shock like synaptosomes. Electron micrographs confirmed that these particles were synaptosomes. The true nature of the small particles remained unclear but morphologically a part of them were also synaptosomes. Treatment of the animals with reserpine (10 mg/kg i.p., 24 h), with 6-hydroxydopamine (100 microgram/rat i.c.v.) or with 5,7-dihydroxytryptamine (200 microgram/rat i.c.v.) did not affect significantly TRH-recovery or distribution in the hypothalamus.     

Functional outline of the epidemic process

The present study has shown that on the level of the parasitic system the epidemic process is a biological system, wherein the host population serves as the internal regulator, the mechanism of transmission serves as the external regulator and the parasite population, as the regulated object. The biological regulating mechanisms of the epidemic process have fundamental differences in the groups of infectious with various mechanisms of transmission, and the specific nature of the mechanism of transmission determines the peculiar features of the biological mechanism which governs the self-regulation of the epidemic process. In contrast, on a higher level of the organization of the epidemic process, i. e. on the level of the socio-ecological system, the epidemic process is a biosocial system, wherein the human society serves as the regulator, the parasitic system serves as the regulated object and the mechanism of transmission plays the role of the filter which determines the scope of social factors, most important in the regulation of the epidemic process in a given infection. The spontaneous regulation of the epidemic process is the freed forward channel from the regulator to the regulated object, and the controlled regulation is the feedback channel.