Mechanism of the development of functional hyperemia in the palatal salivary glands of the rat

At various regimens of the secretory activity in the palatile salivary glands, changes occurring in the transversal profiles of the postcapillary venules, but not of the blood capillaries, are most noticeable. Under food stimulation of secretion, the former dilate essentially, that can demonstrate certain functional hyperemia developing in the palatine salivary glands. Some previous experiments concerning interpretation of principles on the microcirculatory bed spatial organization give a good reason to suggest that dilatation of the postcapillary venules is connected with an increased blood perfusion in the canals of the preferrable blood stream. The postcapillary dilatation is possible because blood from the precapillaries gets into the capacitance blood microvessels and its volume at that moment is greater than the capacity of the venous microvessels. A suggestion is made that filtrative function of the palatile salivary glands depends on development of the functional hyperemia. It is possible, that this mechanism is universal, since owing to it, reflectory reactions of the salivary glands directed to the immediate secure of the oral cavity with a necessary amount of liquor become possible.     

Structural studies on the hexose region of the Enterobacteriaceae type R3 core polysaccharide.

The structure of the hexose region of the Enterobacteriaceae type R3 core polysaccharide, which is the common core in Shigella flexneri and some Escherichia coli lipopolysaccharides (LPS), has been investigated. The principal method used in these studies involved methylation analysis of the original and modified materials. The polysaccharide was modified by N-deacetylation-deamination and by Smith degradation. As a result of these studies, the following structure is proposed: alpha-D-Glcp-(1 leads to 2)-alpha-D-Glcp-(1 leads to 2)-[alpha-D-GlcNAcp-(1 leads to 3)]-alpha-D-Galp-(1 leads to 3)-alpha-D-Glcp-(1 leads to.     

Chemoarchitectonics of metencephalon of Testudo elegant

Histoenzymological study of acid phosphatase (GP-AI), 5-nucleotidase (AMP-A), adenosine triphosphatase (ATP-A) and beta-galactosidase (GLAC-A) of the metencephalon of turtle shows a pattern of distribution of enzymes similar to amphibians and mammalian metencephalon which provides indication of homology of the nuclei and tracts such as nucleus raphe, nuclei cerebelli fasciculus longitudinalis medialis, commissura ansulata and internal arcuate fibers. The nerve fibers, tracts and commissures demonstrate strong activity of GLAC-A as demonstrated in frog and bat by the author in previous studies.     

Modification of rat thymocyte membrane properties by hyperthermia and ionizing radiation.

Thymocytes are one the most widely used cell models for the study of radiation-induced interphase death. This cell-type was chosen for the study of hyperthermic and radiation effects on two membrane-related processes implicated in the interphase death of cells: Na+-dependent 2-aminoisobutyric acid (AIB) transport and cyclic 3'-5' adenosine monophsophate formation. The response of AIB transport to heat is dose-dependent, but the biphasic thermal response curve (AIB uptake versus time) differs fom the sigmoidal radiation response curve. Heating thymocytes for 20-30 min at 43 degrees C stimulates AIB uptake. Additional heating at 43 degrees C, however, markedly reduces AIB uptake. Despite the immediate stimulating effect of heat (30 min at 43 degrees C), the thymocyte has already developed irrepairable impairments, as demonstrated by the fractionated heating experiments. The heat-induced impairment of AIB uptake is mainly on the Na+-dependent component of neutral amino-acid transport, affecting primarily the maximal rate of uptake, i.e. Vmax. Additional evidence for heat-induced plasma membrane damage is the alteration in cAMP levels. Heating thymocytes for 30 min or longer at 43 degrees C causes a massive rise in cAMP level within the cell. This differs from thymocytes exposed to radiation where no rise in cAMP is observed.     

A cellular basis for functionally releasable pools in somatotropes

In an attempt to define the cellular basis for the phenomenon of releasable pools, we compared the effects of two growth hormone (GH)-releasing peptides which differentially influence the dynamics of GH release. Monodispersed anterior pituitary cells from neonatal male rats were subjected to reverse hemolytic plaque assays for GH in the presence or absence of GH-releasing peptide (GHRP-6, an enkephalin-like hexapeptide) and rat GH-releasing factor (GRF). GRF increased the rate of plaque formation (an index of the rate of hormone release) from almost all somatotropes, whereas GHRP-6 influenced only half of these cells. Analysis of plaque sizes (which provides a relative index of the cumulative amount of hormone released per cell) revealed that GRF produced a bimodal frequency distribution of plaque sizes, demonstrating that some somatotropes released more hormone than others after treatment with a maximal dose of this secretagogue. This pattern contrasted with those of untreated and GHRP-6 treated somatotropes which each produced unimodal frequency distributions that were skewed to the left (toward smaller plaques) and were virtually superimposable at the end of a 4 h incubation. However, GHRP-6 greatly accelerated the rate at which the final size distribution pattern was attained. Taken together, these results suggest that GHRP-6 causes the immediate release of a limited pool of GH which is present only in a discrete subpopulation of somatotropes that respond to GRF. This pool may be identical to that which is released over a more prolonged period under basal conditions. Moreover, GRF appears to access a more substantial pool of hormone which is not released by GHRP-6. This pool is present in a small minority of somatotropes but probably accounts for a larger portion of the GH released by pituitaries stimulated with GRF.     

Transmission of experimentally-induced rat virus infection

The duration of transmission of rat virus (RV) infection was determined using Sprague-Dawley rats inoculated oronasally as juveniles (4 weeks old) or as infants (2 days old). Contact transmission from rats inoculated as juveniles was detected for 3 weeks, whereas transmission from rats inoculated as infants occurred for 10 weeks. Transmission continued for at least 7 weeks after seroconversion occurred in rats inoculated as infants. Two of three rats that had ceased to transmit infection harbored infectious virus as detected by explantation of kidney. Intrauterine transmission occurred only after pregnant dams were inoculated with large doses of virus and was more efficient when virus was inoculated intravenously than by the oronasal route. Enzyme immunoassay antibody titers to RV in offspring of previously infected dams decreased steadily during the first 13 weeks of life and 27 of 29 offspring tested by immunofluorescence assay at 12 or 13 weeks of age were seronegative. These results indicate that RV was transmitted by rats inoculated as infants for long periods after seroconversion occurred. They also suggest that the offspring of previously-infected dams were not infected. In utero transmission of RV-Y is unlikely to occur after oronasal inoculation unless rats are exposed to large doses of virus.