scholarly journals FURTHER STUDIES ON THE SUBMAXILLARY GLAND VIRUSES OF RATS AND GUINEA PIGS

1935 ◽  
Vol 62 (6) ◽  
pp. 805-822 ◽  
Author(s):  
Ann G. Kuttner ◽  
T'sun T'ung

1. It has not been possible to increase the virulence of the submaxillary gland viruses of guinea pigs and rats, either by reducing the resistance of the animals by exposure to X-ray, or by the addition of testicular extract (Duran-Reynals factor). 2. In guinea pigs and wild rats with spontaneously infected submaxillary glands, the kidney has been found to contain the virus in the absence of demonstrable pathological changes. 3. Direct injection of these viruses into the kidney produces only mild, circumscribed lesions. 4. The viruses, following subcutaneous injection into white rats and guinea pigs, are widely distributed 2 weeks after injection. They are present in the submaxillary glands, cervical lymph nodes, kidney, and lung. They were not demonstrable at this time in the blood, liver, or spleen. 5. By the intratracheal injection of large doses of virus in guinea pigs and rats, an interstitial bronchopneumonia with thickening of the alveolar and bronchial walls and the presence of acidophilic inclusion bodies, can be produced. 6. No evidence was obtained to indicate that the multiplication of bacteria in the lung is greatly enhanced by the injection of these viruses.

1934 ◽  
Vol 60 (6) ◽  
pp. 773-791 ◽  
Author(s):  
Ann G. Kuttner ◽  
Shao-Hsun Wang

1. Acidophilic intranuclear inclusion bodies occur in the salivary glands of Chinese infants dying from miscellaneous causes. The lesion is similar to that previously described in infants in Europe and America. 2. Attempts to prove that this lesion is due to an infectious agent by its production in animals have been unsuccessful. 3. Acidophilic intranuclear inclusion bodies have been found in the submaxillary glands of hamsters, white mice, and wild rats. 4. Evidence is presented to show that the lesion in hamsters, white mice, and wild rats is due to a virus, which is specific for each species, being transmissible to normal individuals of this breed, and which is very similar to the submaxillary gland virus of guinea pigs.


1927 ◽  
Vol 46 (6) ◽  
pp. 935-956 ◽  
Author(s):  
Ann G. Kuttner

1. It has been shown that the guinea pig virus localizes in the submaxillary glands of young guinea pigs following subcutaneous, intraperitoneal, or intravenous injection of active material, and that the specific lesion is demonstrable in the glands in 12 to 15 days. When an active infection of the gland has been produced in this way, the guinea pigs are refractory to intracerebral inoculation of the virus. 2. No lesion develops in the submaxillary glands of young guinea pigs injected subcutaneously with guinea pig virus which has been inactivated by heat. Young guinea pigs which have received injections of heat-killed virus do not become refractory to intracerebral inoculation of the virus. 3. When young guinea pigs from which both submaxillary glands have been removed are injected subcutaneously with active virus, the virus localizes in the parotid gland, and the animals become refractory to intracerebral inoculation. 4. It has been impossible to demonstrate virucidal properties in the sera of adult guinea pigs which have become spontaneously infected with the virus, or in the sera of young guinea pigs which have been artificially rendered refractory to intracerebral inoculation. 5. It has been possible to transmit the virus from guinea pig to guinea pig continuously in series through seven animals by direct inoculation from submaxillary gland to submaxillary gland. 6. The fact that the virus regularly localizes in the submaxillary glands following subcutaneous inoculation has been utilized in passing the virus from guinea pig to guinea pig. 2 weeks after the subcutaneous inoculation of the virus into young guinea pigs, the active agent was present in the submaxillary glands. Emulsions of the submaxillary glands of these animals were then used for the subcutaneous injection of another group of young guinea pigs. In this way the virus was transmitted continuously from skin to submaxillary gland through a series of seven animals.


1928 ◽  
Vol 47 (2) ◽  
pp. 235-243 ◽  
Author(s):  
Hideyo Noguchi

Bartonella muris appeared in the blood of all white rats, wild rats, Chinese hamster, and mice, from which the spleen was removed, but did not appear in that of splenectomized monkeys, rabbits, or guinea pigs. It has not been possible to transmit B. muris to normal rats, monkeys, rabbits, or guinea pigs, by intraperitoneal, intradermal, or intravenous injection of blood containing B. muris from splenectomized rats. In two instances an acute orchitis was induced in normal rats by injection directly into the testicle of blood or saline suspensions of the liver of splenectomized rats. The intracorpuscular elements occasionally identified as B. muris or as having appeared as a result of the inoculation. The acute orchitis of rats was transferable to normal rats in series. From the testicular tissue, as well as directly from the blood of a splenectomized rat, there was isolated in pure culture a microorganism which induced in the testicles of normal rats an acute orchitis such as resulted from inoculation of the blood or liver suspensions of splenectomized rats. While a few inclusions were found in the erythrocytes of some of the animals, their number was so small and their occurence so infrequent that they could not be definitely identified as B. muris. In morphological features the cultural forms of the microorganism isolated resemble B. muris. The organism found in the testicular tissues, however, is considerably coarser than B. muris and takes a deeper stain. Immunological study failed to settle the question of the relation between B. muris and the cultivated organism, which is provisionally called Bacterium murium. Bartonella muris, Bartonella bacilliformis, and Grahamella talpæ have characteristic individual morphological features.


1932 ◽  
Vol 55 (3) ◽  
pp. 405-415 ◽  
Author(s):  
N. Paul Hudson ◽  
Floyd S. Markham

The submaxillary gland virus of guinea pigs was serially transmitted from brain to brain in young guinea pigs. The source of virus was the submaxillary glands of six groups of stock animals. Brain to brain transfer was effected in two series, in one to the second generation and in the other to the third. The transmission was evidenced by the presence of nervous symptoms and death and by a typical microscopic pathology of the brain. Only certain attempts were successful, ten of twenty-three brain to brain injections being fatal with the specific histopathology present in five. A few observations suggest that the virus may be present spontaneously in the gland and experimentally in the brain without cellular changes being demonstrable, or before they are evident. While we were able to transmit the virus from brain to brain with fatal results by single injections of small doses, this was not readily accomplished and the transmission failed after two or three passages. We were unable to show any perceptible increase in virulence or adaptation of the virus to the brain tissue of the natural host. The histopathology was that of a meningoencephalitis. The inflammatory reaction irregularly involved the meninges, the underlying brain substance, and the perivascular tissue of the meninges and upper cortical layer. These structures were infiltrated with mononuclear cells, many of which contained a typical acidophilic inclusion. Congestion of cerebral capillaries uniformly occurred and various degrees of recent hemorrhage were frequently found. Necrosis was noted only when associated with an occasional area of extensive hemorrhage. Similar changes were observed in sections of the spinal cord. When sufficient time (15 days or more) elapsed between cerebral inoculation and death, typical cellular inclusions were seen in the salivary glands, whereas none was found in animals that died earlier (7 to 9 days). Under the first mentioned conditions, inclusions were demonstrated in the parotid and mucous portion of the submaxillary glands, although in spontaneously infected animals, we failed to find the mucous portion involved and other workers report that the parotid is spared. About one-third of the stock guinea pigs examined showed cellular inclusions in both the nucleus and cytoplasm of epithelial duct cells of the serous part of the submaxillary gland. From an analysis of the results of brain to brain inoculations, it was evident that spontaneous infection and resistance to cerebral inoculation increased with age. The 3rd week of life is the period of choice for such experimentation.


1984 ◽  
Vol 259 (20) ◽  
pp. 12714-12717
Author(s):  
M A Navia ◽  
J P Springer ◽  
M Poe ◽  
J Boger ◽  
K Hoogsteen

1953 ◽  
Vol 97 (5) ◽  
pp. 663-680 ◽  
Author(s):  
Charles Huggins ◽  
John Lambert Sommer

The prostate of the dog was relocated permanently in the perineum where its size could be measured and correlated with the output of prostatic secretion during many months. The secretion of a submaxillary gland obtained through a fistula was utilized as an internal biologic standard of the effects of pilocarpine, the secretory stimulus employed, because the amount and route of administration of the alkaloid are critical factors in inducing secretion. Prostatic secretion was found to be profoundly affected by androgenic and estrogenic compounds, in contrast to salivation. The curves of the secretory response of the prostate and submaxillary glands to pilocarpine proved to be similar and a mathematical formula has been constructed to represent them. When testosterone propionate was administered in increasing quantities for periods of weeks at each level, the volume of the prostate increased in a series of flattened curves. This volume, under the conditions mentioned, was found to stand in a simple arithmetic relationship to the amount of testosterone propionate administered. Moderate quantities of testosterone propionate masked the effects of small amounts of stilbestrol on the prostate. The reverse was also true and the critical amounts of these compounds were defined. The amounts of stilbestrol were determined which lowered the quantity of prostatic secretion resulting from the simultaneous administration of moderate amounts of testosterone propionate in castrate dogs, the result being a level and flat secretory curve which was maintained for many weeks. We designate this effect the plateau phenomenon. When this amount of estrogen was continued, and the dosage of testosterone propionate greatly augmented, the prostatic secretion did not increase in volume. Very slight increases above the critical amount of stilbestrol, however, caused the secretory curve to fall to new and still lower levels though the secretion was never completely suppressed. The acid phosphatase content of the prostatic secretion in the regions of secretory plateaus was similar to that of castrate dogs injected with androgen alone. The plateau phenomenon is due to simultaneous physiologic action of androgenic and estrogenic compounds on the prostatic cells. The depression of prostatic secretion resulting in the plateau phenomenon is due to both functional and structural changes in the prostatic epithelium. They are best explained on the assumption that differences in steroid threshold exist in groups of cells within the prostate, those of the anterior rim of the gland being least susceptible to estrogenic activity.


2001 ◽  
Vol 169 (2) ◽  
pp. 389-396 ◽  
Author(s):  
A Perez-Romero ◽  
E Dialynas ◽  
F Salame ◽  
A Amores ◽  
L Vidarte ◽  
...  

High local GH-releasing hormone (GHRH) levels are capable of inducing transdifferentiation in salivary cells to synthesize GH. However, the factors implicated in this process remain unknown. To study this subject, normal and Ames dwarf mice were implanted in the submaxillary gland with a slow release pellet releasing 21 microgram GHRH (1-29)-NH(2)/day for 2 months. Control animals received placebo pellets at the same site. After 60 days, heart blood was collected and submaxillary glands were removed. Circulating levels of GH and IGF-I were significantly decreased (P<0.05) in dwarf mice in comparison with controls, and GHRH treatment did not modify either of these two parameters. Controls carrying GHRH pellets showed a significantly higher GH content (P<0.05) in the submaxillary gland than the placebo-treated normal mice. There were no differences between the IGF-I concentrations of placebo- and GHRH-treated salivary tissue from normal mice. Analysis of GH mRNA by RT-PCR followed by Southern blot revealed that GH transcripts were present in the salivary gland samples carrying the placebo pellets in both normal and dwarf mice. The expression of GH was significantly (P<0.05) increased by the GHRH pellets in salivary tissue from normal mice, but not in submaxillary glands from dwarf mice. Pit-1 mRNA was not detected in the GHRH-treated glands of normal and dwarf mice by RT-PCR or by Southern blot. Using these highly sensitive methods, we have been able to detect the transcription of both GH and Pit-1 in pituitaries from Pit-1-deficient Ames dwarf mice. The present experiment demonstrates that salivary tissue synthesizes GH when it is exposed to the influence of GHRH. Both basal and GHRH-induced salivary GH expression appear to be independent of Pit-1.


1917 ◽  
Vol 25 (1) ◽  
pp. 33-44 ◽  
Author(s):  
Kenzo Futaki ◽  
Itsuma Takaki ◽  
Tenji Taniguchi ◽  
Shimpachi Osumi

1. Since our first report on the discovery of the cause of rat-bite fever, we have been able to prove the existence of the same spirochete in five out of six more cases which have come under our observation. 2. The clinical symptoms of rat-bite fever are inflammation of the bitten parts, paroxysms of fever of the relapsing type, swelling of the lymph glands, and eruption of the skin, all occurring after an incubation period usually of from 10 to 22 days, or longer. 3. Our spirochete is present in the swollen local lesion of the skin and the enlarged lymph glands. But as the spirochetes are so few in number it is exceedingly difficult to discover them directly in material taken from patients. It is therefore better to inoculate the material into a mouse. In some cases the organism is found in the blood of the inoculated animal after a lapse of 5 to 14 days, or at the latest 4 weeks. 4. Generally speaking, the spirochetes present thick and short forms of about 2 to 5 µ and have flagella at both ends. Including the flagella, they measure 6 to 10 µ in length. Some forms in the cultures reach 12 to 19 µ excluding the flagella. The curves are regular, and the majority have one curve in 1 µ. Smaller ones are found in the blood and larger ones in the tissues. 5. The spirochetes stain easily. With Giemsa's stain they take a deep violet-red; they also stain with ordinary aniline dyes. The flagella, too, take Giemsa's stain. 6. The movements of our spirochetes are very rapid, resembling those of a vibrio, and distinguish them from all other kinds of spirochetes. When, however, the movements become a little sluggish, they begin to present movements characteristic of ordinary spirochetes. 7. For experimental purposes, mice, house rats, white rats, and monkeys are the most suitable animals. Monkeys have intermittent fever after infection, and spirochetes can be found in their blood, but they are not so numerous as in the blood of mice. Mice are the most suitable animals for these experiments, and they appear, as a rule, to escape fatal consequences. 8. The spirochete is markedly affected by salvarsan. 9. The organism is not present in the blood of all rats, and there is no relation between the species of the rat and the ratio of infection. We have never found the spirochete in healthy guinea pigs or mice. By permitting a rat infected with the spirochete to bite a guinea pig, the latter develops the disease. 10. We have succeeded in cultivating the spirochete in Shimamine's medium. 11. Among the spirochetes described in the literature or discovered in the blood of rats and mice, there may be some resembling our spirochete, but none of the descriptions agree with it fully. Hence we have named our organism Spirochæta morsus muris and regard it as belonging to the Spironemacea (Gross) of the nature of treponema. 12. The spirochete can be detected in the bodies of patients. In seven cases out of eight, it disappears on recovery, only to reappear during the relapse. 13. The spirochete can be detected in about 3 per cent of house rats. These facts enable us to identify the cause of the disease. 14. There may be other causes than the spirochete for diseases following the bite of a rat. The cause, however, of rat-bite fever in the form most common in Japan is, we believe, the spirochete which we have described.


Development ◽  
1981 ◽  
Vol 62 (1) ◽  
pp. 229-239
Author(s):  
Hiroyuki Nogawa

Quail anterior submaxillary glands elongated extensively without branching (more than sevenfold) from 8 to 10 incubation days. Investigation of mitotic activity of the rudiments in vivo showed no localized cell proliferation throughout the rudiments, and recombination experiments in vitro to examine regional differences in mitogenic activity of the surrounding mesenchyme also showed that no mesenchymal region specifically stimulates the epithelial cell proliferation. Histological observation of the rudiments showed that epithelial cells did not lengthen in a parallel direction to the long axis of the rudiment, and that mesenchymal cells encircled the epithelial cord perpendicularly to its axis. The basement membrane was obscure in the distal end of the rudiments, while it was easily detected in the other part of the rudiments. These results suggest that the elongating morphogenesis of the anterior submaxillary rudiments is not achieved by localized cell proliferation but by almost uniformly distributed cell proliferation, and mesenchymal cells surrounding the rudiment or the basement membrane may be involved in the controlling mechanisms of the elongating morphogenesis.


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