THE INFLUENCE OF OESTRIOL AND PROGESTERONE ON THE ENDOMETRIUM OF THE GUINEA-PIG IN VITRO

1962 ◽  
Vol 24 (4) ◽  
pp. 491-NP ◽  
Author(s):  
JANET EVERETT

SUMMARY The direct influence of oestriol and progesterone, and a combination of these hormones, on endometrium of guinea-pigs has been studied in organ culture. Progesterone stimulated the size and number of stromal cells, and provoked slight dilation of uterine glands. The glands were more numerous and widely dilated in the presence of oestriol, and the number and size of stromal cells were even greater than with progesterone alone. A combination of the two hormones led to the simultaneous appearance of synergism—well-preserved epithelium and glands of a secretory nature, and antagonism—there being fewer stromal cells of a smaller size than with either hormone alone. The significance of these results is discussed in relation to the effects of the hormones in vivo. The inhibitory action of progesterone on the appearance of the cystic hyperplasia of the uterine glands provoked by oestriol was noted.

1976 ◽  
Vol 36 (02) ◽  
pp. 401-410 ◽  
Author(s):  
Buichi Fujttani ◽  
Toshimichi Tsuboi ◽  
Kazuko Takeno ◽  
Kouichi Yoshida ◽  
Masanao Shimizu

SummaryThe differences among human, rabbit and guinea-pig platelet adhesiveness as for inhibitions by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid are described, and the influence of measurement conditions on platelet adhesiveness is also reported. Platelet adhesiveness of human and animal species decreased with an increase of heparin concentrations and an increase of flow rate of blood passing through a glass bead column. Human and rabbit platelet adhesiveness was inhibited in vitro by adenosine, dipyridamole and chlorpromazine, but not by acetylsalicylic acid. On the other hand, guinea-pig platelet adhesiveness was inhibited by the four drugs including acetylsalicylic acid. In in vivo study, adenosine, dipyridamole and chlorpromazine inhibited platelet adhesiveness in rabbits and guinea-pigs. Acetylsalicylic acid showed the inhibitory effect in guinea-pigs, but not in rabbits.


1937 ◽  
Vol 37 (3) ◽  
pp. 471-473 ◽  
Author(s):  
J. Gordon ◽  
N. Wood

In earlier papers (Gordon, 1930) it was shown that congo red has an inactivating effect on serum complement, both haemolytic and bactericidal, and that this effect can be reversed by treating the serum and congo red mixture with charcoal, the charcoal removing the congo red and leaving the complement active again. A similar reversal of inactivation is obtained by using instead of the charcoal, heated serum (55° C. for 30 min.) or protein solutions. Later (Gordon, 1931), it was shown that congo red had an inactivating effect on the haemolysins of Streptococcus haemolyticus and B. welchii. The reversibility of this effect was not so easy to demonstrate as with complement. Charcoal had a destructive effect on the haemolysins and so could not be used. It was found, however, that when the concentration of congo red was just sufficient to neutralize the streptococcal haemolysin, the addition of cuprammonium artificial silk adsorbed the congo red and liberated the haemolysin. In the case of B. welchii this method of reversal was not suitable, as the artificial silk had a destructive effect on the haemolysin. Instead, reversibility was demonstrated by adding ox serum to the mixture of congo red and haemolysin. This brought about a redistribution of the congo red between the ox serum and the haemolysin and if the amount of congo red used had been only just sufficient to neutralize the haemolysin of B. welchii, then the haemolytic activity could again be demonstrated. Gordon and Robson (1933) showed that congo red interfered with the anaphylactic reaction tested both in vivo and in vitro, the guinea-pig uterus being used in the in vitro experiments, in which the inhibitory action of the dye was shown to be reversible. It was suggested that the congo red interfered with the entrance of antigen into the cell.


1977 ◽  
Vol 6 (4) ◽  
pp. 355-371 ◽  
Author(s):  
Zvi H. Marcus ◽  
Yael Shtal ◽  
Gerald Dominique ◽  
Laslo Nebel
Keyword(s):  

1994 ◽  
Vol 179 (3) ◽  
pp. 881-887 ◽  
Author(s):  
P J Jose ◽  
D A Griffiths-Johnson ◽  
P D Collins ◽  
D T Walsh ◽  
R Moqbel ◽  
...  

Eosinophil accumulation is a prominent feature of allergic inflammatory reactions, such as those occurring in the lung of the allergic asthmatic, but the endogenous chemoattractants involved have not been identified. We have investigated this in an established model of allergic inflammation, using in vivo systems both to generate and assay relevant activity. Bronchoalveolar lavage (BAL) fluid was taken from sensitized guinea pigs at intervals after aerosol challenge with ovalbumin. BAL fluid was injected intradermally in unsensitized assay guinea pigs and the accumulation of intravenously injected 111In-eosinophils was measured. Activity was detected at 30 min after allergen challenge, peaking from 3 to 6 h and declining to low levels by 24 h. 3-h BAL fluid was purified using high performance liquid chromatography techniques in conjunction with the skin assay. Microsequencing revealed a novel protein from the C-C branch of the platelet factor 4 superfamily of chemotactic cytokines. The protein, "eotaxin," exhibits homology of 53% with human MCP-1, 44% with guinea pig MCP-1, 31% with human MIP-1 alpha, and 26% with human RANTES. Laser desorption time of flight mass analysis gave four different signals (8.15, 8.38, 8.81, and 9.03 kD), probably reflecting differential O-glycosylation. Eotaxin was highly potent, inducing substantial 111In-eosinophil accumulation at a 1-2 pmol dose in the skin, but did not induce significant 111In-neutrophil accumulation. Eotaxin was a potent stimulator of both guinea pig and human eosinophils in vitro. Human recombinant RANTES, MIP-1 alpha, and MCP-1 were all inactive in inducing 111In-eosinophil accumulation in guinea pig skin; however, evidence was obtained that eotaxin shares a binding site with RANTES on guinea pig eosinophils. This is the first description of a potent eosinophil chemoattractant cytokine generated in vivo and suggests the possibility that similar molecules may be important in the human asthmatic lung.


1990 ◽  
Vol 63 (03) ◽  
pp. 459-463 ◽  
Author(s):  
S Wilson ◽  
P Chamberlain ◽  
I Dodd ◽  
A Esmail ◽  
J H Robinson

SummaryA hybrid plasminogen activator consisting of the “A” chain of plasmin linked to the “B” chain of rt-PA was inhibited in vitro in human and guinea pig plasmas 4 to 5-fold more rapidly than its parent activator, two-chain t-PA. Using zymographic and autoradiographic techniques together with the use of immunodepleted plasma the major inhibitor was identified as aIpha-2-antiplasmin. The pharmacokinetic profile of the hybrid in guinea pigs was determined by two different methods: disappearance of fibrinolytic activity and removal of radiolabelled hybrid from the circulation. Fibrinolytic activity was cleared rapidly via inhibitory mechanisms, whilst radiolabelled material was cleared considerably more slowly due to the formation of hybrid-inhibitor complexes. When the active site of the hybrid was reversibly acylated inhibitory mechanisms were evaded and a prolonged pharmacokinetic profile of activity was observed.


2018 ◽  
Vol 5 (suppl_1) ◽  
pp. S16-S16
Author(s):  
Cody Ruhl ◽  
Lexy Kindt ◽  
Haaris Khan ◽  
Chelsea E Stamm ◽  
Breanna Pasko ◽  
...  

Abstract Background A hallmark symptom of active pulmonary tuberculosis vital for disease transmission is cough. The current paradigm for tuberculosis-related cough is that it results from airway damage or irritation. However, there is limited experimental data to support this theory, and whether Mycobacterium tuberculosis (Mtb) induces cough to facilitate its own transmission has not been explored. The cough reflex is a complex and coordinated event involving both the nervous and musculoskeletal systems initiated by particulate or chemical molecules activating nociceptive neurons, which sense pain or irritation. This activation induces a signaling cascade ultimately resulting in a cough. Respiratory nociceptive neurons innervate the airway of humans and most mammals, and thus are poised to respond to noxious molecules to help protect the lung from damage. Because Mtb is a lung pathogen, cough is a primary mechanism of Mtb transmission, and respiratory nociceptive neurons activate cough, we hypothesized that Mtb produces molecules that stimulate cough, thereby facilitating its spread from infected to uninfected individuals. Methods We used an in vitro neuronal activation bioassay to fractionate, identify, and characterize Mtb cough-inducing molecules. We also measured cough in vivo in response to pure Mtb-derived cough molecules and during Mtb infection using a guinea pig model. Results We found that an acellular organic extract of Mtb triggers and activates nociceptive neurons in vitro with a neuronal response that is as robust as the response to capsaicin, an established nociceptive and cough-inducing molecule. Using analytical chemistry and our neuronal bioassay, we then isolated 2 molecules produced by Mtb that activate nociceptive neurons. Both the organic Mtb extract and purified molecules alone were sufficient to induce cough in a conscious guinea pig cough model. Finally guinea pigs infected with wild-type Mtb cough much more frequently than guinea pigs infected with Mtb strains unable to produce nociceptive molecules. Conclusion We conclude that Mtb produces molecules that activate nociceptive neurons and induce cough. These findings have significant implications for our understanding of Mtb transmission. Disclosures All authors: No reported disclosures.


Parasitology ◽  
1983 ◽  
Vol 87 (3) ◽  
pp. 465-479 ◽  
Author(s):  
E. J. Pearce ◽  
Diane J. McLaren

SummaryIn vivoandin vitroparameters of immunity have been assessed in guinea-pigs sensitized with 500 normal or 500 radiation-attenuated cercariae ofSchistosoma mansoni. High levels of resistance to a challenge infection developed in both the chronic and irradiated vaccine model, but immunity was expressed earlier (week 4) and reached higher levels (90%) in the latter case. Vaccinated guinea-pigs have thus been shown to achieve greater resistance than the more commonly used rodent hosts.In vitrocytotoxicity assays have demonstrated that antibodies capable of participating in complement-dependent (lethal antibody) or eosinophil-mediated schistosomular killing, develop in the serum of guinea-pigs immunized with either normal or irradiated cercariae. The time course of development of the eosinophil adherence promoting antibody approximated in both models, the development of immunityin vivo, but the lethal antibody response paralleled the immune status of the animal only in the irradiated vaccine model


Diphtheria antitoxin prepared in the horse and refined by peptic digestion when injected in very large doses into women in an advanced stage of pregnancy did not pass to the infant. In pregnant guinea-pigs diphtheria antitoxin (naturalserum, ex -guinea-pig) passed to the young in abundance; but, after peptic-digestion, this homologous antitoxin failed entirely to pass the placenta, the young being devoid of antitoxin at birth. The passage was not affected by the treatment of the natural serum with ammonium sulphate as used in the Gibson-Banzhaf (1910) process for the concentration of antitoxin. Diphtheria antitoxin (natural serum ex -horse) passed from pregnant guinea-pigs to their off spring in smaller amounts and much less readily than homologous antitoxin, and the quantity of antitoxin( ex -horse) so passing was reduced even further and very considerably as a result of peptic digestion. Even under the most favourable conditions homologous antitoxin takes sometime (2 or 3 days) to attain the same concentration in the young as in the mother; but once this concentration has been attained it is preserve data high level for long periods. Passive anaphylactics ensitization of guinea-pigs, either of the whole animal or the isolated uterus, is easily effected, in vivo or in vitro , by small quantities of diphtheria antitoxin (either natural serum or ammonium sulphate concentrated, ex -guinea-pig), but this property is completely lost when the homologous antitoxin is subjected to peptic digestion. It is not possible to sensitize anaphylactically guinea-pigs, in vivo or in vitro , by means of diphtheria antitoxin, ex -horse, whether the antibody is presented either in the form of natural serum, or concentrated by means of ammonium sulphate; and the result is the same when pepsin-refined diphtheria antitoxin ex -horse is used. When 5 or 10 units of diphtheria antitoxin ex -horse, whether as natural serum, ammonium-sulphate concentrated or pepsin-refined, are injected subcutaneously into guinea-pigs, the animals are rendered Schick-negative in a few hours. These antitoxins are eliminated in about a week, after which time the injected guinea-pigs are found to be Schick-positive again. If, however, the same amounts of antitoxin made in guinea-pigs are injected into guinea-pigs the result is different; the animals also become Schick-negative, but this condition is maintained for a month or longer. That is, homologous antitoxin is eliminated much more slowly; but if this natural serum antitoxin from the guinea-pig is subjected to peptic digestion it is eliminated as quickly as diphtheria antitoxin made in the horse. When diphtheria toxin is injected intracutaneously into guinea-pigs, a quantity of diphtheria antitoxin 50,000 times as large as that required to neutralize it in vitro is required for neutralization in the animal, and then only if injected intravenously within 1hr.; but little or no neutralization in vivo occurs if the intravenous injection is longer delayed, whatever type of homologous or heterologous antitoxin is administered.


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