ETIOLOGIC CONSIDERATIONS OF SPONTANEOUS TUMORS IN ANIMALS WITH SPECIAL REFERENCE TO THE ENDOCRINE SYSTEM.
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Pituitary-thyroid axis function and gonadotropin secretion were evaluated by a combined TRH and LHRH test in 4 newborn female infants appropriate for gestational age of mothers treated by AEDs throughout pregnancy. We found: high basal FSH levels with normal FSH reserve, normal LH-HCG levels both before and after LHRH stimulation, normal TSH and T4 levels both before and after TRH stimulation, high T3 basal values with a normal increase after TRH and low rT3 basal values. It is suggested an AED increased T4 deiodination towards T3 in the newborn liver without a marked impairment of the endocrine functions of the fetus.
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Nitrite is a harmful substance generated in Litopenaeus vannamei farming systems, largely originating from the inadequate breakdown of surplus feed and shrimp feces. Its accumulation in the water can affect the growth and physiological functions of shrimp, damage the immune system, and even cause mass mortality, thus becoming a key environmental factor restricting the green development of the industry. Under nitrite stress, the eyestalk, as an important neuroendocrine regulatory center in crustaceans, participates in the stress adaptation of the organism and exerts a protective effect by regulating energy metabolism and immune function. However, the molecular regulatory mechanism of the eyestalk in response to nitrite stress remains unclear. In this study, single-cell RNA sequencing (scRNA-seq) technology was used to analyze the heterogeneity of eyestalk cells in L. vannamei under nitrite stress. A total of 18, 394 high-quality cells were obtained, and six major cell subpopulations, including Neurosecretory cell, Motor neuron, Sensory neuron, Interneuron, Neurogliocyte, and Support cell, were identified. Differential expression analysis identified 839 differentially expressed genes, and different cell types showed distinct specific responses to nitrite stress. Functional enrichment analysis indicated that pathways such as glycolysis, oxidative phosphorylation, ribosome function, and endoplasmic reticulum protein processing were significantly activated, while signal transduction and DNA repair-related pathways were inhibited. Further analysis revealed that nitrite stress could induce mitochondrial function changes and trigger oxidative stress, thereby affecting the neuroendocrine system function of the eyestalk. This study provided insights into transcriptomic responses of the eyestalk to nitrite stress at the single-cell level, laying a theoretical foundation for the management of aquaculture environments.
The repeated administration of 3-methylcholanthrene to adolescent rats resulted in (a) a profound, incomplete, and selective depression of certain hypophyseal functions; (b) decreased growth of transplanted mammary tumors; and (c) a retardation of body growth. Only the last mentioned effect was reversed by forced feeding. The retarded rate of body growth induced by 3-methylcholanthrene was prevented by the concurrent administration of dihydrotestosterone or progesterone, or by ovariectomy; rats so treated became overweight despite the injection of 3-methylcholanthrene. Phenolic estrogens intensified the retardation of body growth induced by 3-methylcholanthrene and emaciation resulted. The administration of 3-methylcholanthrene resulted in decreased gonadotrophin production by the pituitary and the ovaries were more drastically affected by the depression of pituitary activity than the adrenals were. The compound exerted differential effects on the pituitary glands of males and females respectively. Hormonal functions of both ovary and testis were decreased in rats treated with 3-methylcholanthrene but, whilst ovarian weight was much reduced, the size of the testis was not decreased and the germinal epithelium of the male was little affected by the treatment in most instances. There was a considerable reduction of the content of alkaline phosphatase in the breast of intact rats treated with 3-methylcholanthrene but atrophy of the mammary epithelium did not occur and hyperplasia of the mammary tree was often observed. The administration of 3-methylcholanthrene considerably slowed the growth of transplanted mammary tumors characterized by high dependence on hormones and the concurrent administration of gonadotrophin restored the growth rate of the tumors. The administration of 3-methylcholanthrene or androstan-17beta-ol-3-one was only moderately effective in controlling the growth of transplanted mammary tumors characterized by low hormonal dependence; the combined administration of these compounds was highly efficacious in retarding the growth of these refractory tumors. 3-Methylcholanthrene partially retarded the growth of mammary fibroadenomas in hypophysectomized rats.
The proper function of the normal human endometrium relies on well organized cell-cell interactions regulated locally by cytokines and growth factors under the direction of steroid hormones. The onset and progression of the disease processes of endometriosis may result from disruptions of this well balanced cellular equilibrium. Evidence continues to accumulate indicating that environmental toxins, whether naturally occurring or man-made, may directly (hormone disruptor) or indirectly (immune toxin) affect the response of the endometrium to steroids, resulting in various pathological states including endometriosis.
Although adipose tissue has long been considered to be metabolically passive and primarily responsible for energy storage, recent scientific advances have dramatically altered our understanding of the function of this ubiquitous tissue. The fat cell is a transducer of energy supply for the changing metabolic needs of the body, modulating glucose homeostasis, hypothalamic function, sympathetic output, vascular tone, immune response, and reproduction. Through endocrine/autocrine and paracrine actions, adipocyte-derived molecules defend the body during periods of energy deficit and stress. With the development of obesity, maladaptive responses to adipose excess result in pathologic states of inflammation, coagulopathy, and altered insulin sensitivity.
Over the past few years, significant progress has been made in characterizing the expression and localization of proteins that act as scaffolds for cAMP-dependent protein kinase (PK-A). These A-kinase anchor proteins (AKAPs) tether PK-A to intracellular organelles and structures, sequestering the kinase near its physiological substrates. The compartmentalization of distinct pockets of PK-A activity serves to provide spatial regulation of this signaling pathway. In addition, other signaling proteins bind to AKAPs, as do some newly described proteins of unknown function, suggesting that proteins of various pathways are anchored through AKAPs.