Diseases of truck crops and their control

Taubenhaus, J. J.

doi:10.5962/bhl.title.40418

Cited by 4 publications

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“…Our findings, therefore, are only in partial agreement with those obtained by Taubenhaus and Amromin (6,7) in the rat. Their method to produce granulation tissue, however, was different from ours, mainly because of the use of turpentine whose possible action on connective tissue is not well known and because of the presence of a large number of polymorphonuclear leucocytes near the grunulation tissue.…”

Section: Discussionsupporting

confidence: 75%

“…This view seems also to be compatible with the known action of cortisone on connective tissue. This hormone when administered in large amounts inhibits mesenchymal cell proliferation and production of intercellular material (39,40,7). It would seem possible that a lack or diminished output of cortisone may be followed by the opposite phenomenon, i.e., excessive mesenchymal cell proliferation and production of intercellular material.…”

Section: Discussionmentioning

confidence: 99%

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Desoxycorticosterone Acetate and Wound Healing

Pirani

Stepto

Sutherland

1951

Journal of Experimental Medicine

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According to Selye and coworkers (1-3) overdosage of desoxycorticosterone acetate (DCA) in the rat may induce changes characterized by nephrosclerosis with hypertension and by cardiovascular and articular lesions of the "rheumatic type." On the basis of his experiments Selye (4, S) theorized that certain chronic diseases, such as rheumatic fever, periarteritis nodosa, arthritis, and hypertension, are the result of an abnormal response or of a perverted adaptation to stress mediated through the endocrine system, particularly an overproduction of adrenocortical hormones or hypercorticism. These conditions, which are all known to involve mainly tissues of mesenchymal origin, were therefore classified by Selye as "diseases of adaptation."Recently Taubenhaus and Amromin (6) reported that DCA stimulates the proliferation of fibroblasts and encourages the deposition of a homogeneous groundwork of collagen. They obtained these results by studying the effect of the hormone on the granulation tissue around subcutaneous turpentine abscesses in rats. On the basis of more recent studies (7) these investigators advanced the opinion that the stimulating effect of DCA may take place through mechanisms other than direct influence upon granulation tissue. The possibility that the action of DCA is mediated through an enzymatic mechanism must be considered especially in view of observations (8, 9) pointing to the important role of alkaline phosphatase in the proliferation of tissues of mesenchymal origin, and of other studies (10) indicating that DCA increases the activity of alkaline phosphatase in the epiphyses of rats' femora. The effect of DCA administration on other factors which influence mesenchymal cell proliferation, such as ascorbic acid metabolism and adrenocortical function, must also be considered in this respect.Previous unpublished studies from our laboratory (11) on the effect of large doses of DCA in intact guinea pigs showed that, as in the rat (4, 5), the main lesions attributable to this hormone are localized in the cardiovascular-renal system and in the adrenals. These changes consist of moderate to severe nephro-* The opinions expressed in this paper are those of the authors, and do not necessarily represent the official views of any governmental agency.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Desoxycorticosterone Acetate and Wound Healing

Pirani

Stepto

Sutherland

1951

Journal of Experimental Medicine

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“…The increase in hypersensitivity in this instance was also preceded by a delay of several days and it was suggested that an increased secretion of thyroxine was responsible, this hormone having an action opposed to that of cortisone. Since thyroxine has been shown to promote the development of granulation tissue in hypophysectomised rats (Taubenhaus & Amromin, 1950) although not in intact animals (Taubenhaus, Taylor & Morton, 1952) it is possible that it may be implicated in the increased inflammatory response 7 days after adrenalectomy. On the other hand Spencer & West (1963), who studied the relationship between the thyroid and adrenal glands and their effect on histamine metabolism in the rat, concluded that there was no true balance between the glands, the anti-cortisone action of thyroxine being indirect and mediated via an alteration in the amount of corticosteroid available to the tissues.…”

Section: Discussionmentioning

confidence: 99%

Effect of adrenalectomy on cotton pellet granuloma formation in the rat

Ashford¹,

Penn²

1965

Journal of Pharmacy and Pharmacology

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The development of granulomas over 3 days was inhibited in adrenalectomised rats when cotton pellets were implanted on the day of adrenalectomy and was potentiated when the pellets were implanted 7 days after adrenalectomy. The initial inhibitory effect of adrenalectomy was not observed when the granulomas were allowed to remain in situ for 7 days instead of 3 days and was completely reversed by treatment with corticosterone.LTHOUGH the actions of adrenal hormones on developing granula-A tion tissue are widely known, there is some confusion about the effect of adrenalectomy upon healing wounds and granuloma formation. Whereas it has been reported that healing was retarded in adrenalectomised animals (Selye, 1947;Clayton & Prunty, 1951) and that the formation of granulomas around turpentine-induced abscesses in the rat was inhibited by adrenalectomy (Taubenhaus & Amromin, 1950), other workers have found that the amount of tissue formed around an implanted ivalon sponge (Pernokas, Edwards & Dunphy, 1957) or around a plastic ring (Jorgensen, 1962) Our observations show that effects of adrenalectomy ranging from inhibition to potentiation of granuloma formation can be elicited in the rat and are dependant upon the time that elapses between adrenalectomy and implantation of the irritant material. Experimental METHODSFemale Wistar rats, 130 and 180 g weight, were bilaterally adrenalectomised through a dorsal incision under ether anaesthesia. Controls were sham operated and non-operated animals ; the latter were given ether only. The room temperature was 27" and the adrenalectomised animals received 0.9% saline to drink instead of tap water, Sterile cotton pellets each weighing between 6 and 10 mg (Johnson and Johnson) were implanted one in each groin under ether anaesthesia. Each batch of pellets was screened for irritancy since they varied in this property. The time of implantation in relation to adrenalectomy varied and is stated in the text (day 0 = implantation immmediately after adrenalectomy).

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“…If aflatoxin forms only in storage, its formation could be prevented by proper handling-for example, by maintaining moisture levels below 15% and avoiding excessive breakage. There is evidence of aflatoxin formation in storage, but the possibility of toxin formation in the field could not be ignored because of a 1920 report by Taubenhaus of an invasion of field corn by A. flavus in Texas (30). The presence erA.…”

mentioning

confidence: 99%

“…Taubenhaus (30) first reported that A. flavus infection of field corn was frequently associated with corn earworm damage 9 The incidence of A. flavus on kernels from ears damaged by earworms, borers, mites, and stinkbugs was found to be significantly higher (5 9149 than on those from undamaged ears (2 9 (31). There has been some evidence that aflatoxin incidence could be related to earworm damage (34) or to European corn borer infestation (35).…”

mentioning

confidence: 99%

Aflatoxin in corn

Shotwell

1977

J Americ Oil Chem Soc

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and Summary Low incidence and levels of aflatoxin were identified in corn of all grades grown in the Midwest in 1964, 1965, and 1967. Later surveys indicate that corn grown in southern regions is subject to invasion byAspergillus flavus and subsequent aflatoxin formation. This mycotoxin is formed either in the field or in storage. In the field, such factors as insect damage and weather conditions probably influence aflatoxin formation. In storage, temperatures must be above 25 C and moisture levels above 16% if toxin is to form. Aflatoxin formed in a hot spot in stored corn in the Midwest when temperatures rose early in the summer and when the grain became wet because of leaks in the storage building. Analytical methods to detect and determine aflatoxin fall into three categories: presumptive tests indicating the presence ofA. flavus and the possible occurrence of aflatoxin, rapid screening tests establishing the presence or absence of the toxin, and quantitative procedures determining toxin levels. Detoxification methods being studied include ammoniation and roasting. Ammoniated corn is being fed domestic animals to determine whether it has adverse effects and whether toxic compounds are transmitted in animal tissues.

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Diseases of truck crops and their control

Cited by 4 publications

References 0 publications

Desoxycorticosterone Acetate and Wound Healing

Desoxycorticosterone Acetate and Wound Healing

Effect of adrenalectomy on cotton pellet granuloma formation in the rat

Aflatoxin in corn

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