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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Few studies have referred to the implication of apoptotic processes following hormonal treatment. No data are available on the effects of progesterone in breast cells. In order to gain insights on the effects of the gonadal steroids and antiestrogens in breast cells, we have carried out studies on apoptosis in different breast materials. We have developed a model of normal breast cells in cultures that remain hormone-dependent. On these cells and in some hormone-dependent breast cancer cell lines (T-47-D, ZR75-1, MCF-7) we have observed an antiapoptotic effect of estradiol (E(2)) and a potent proapoptotic effect of some antiestrogens. Progestins were also proapoptotic in normal as well as in hormone-dependent breast cancer cells. In order to understand the mechanisms of these hormones on apoptosis, we studied the bcl-2 family proteins. We demonstrated that E(2) increased the antiapoptotic proteins, bcl-2 and bclx(L), whereas, the progestins drastically decreased bcl-2 expression and weakly bclx(L) levels. We investigated the mechanisms by which E(2) increased bcl-2 expression. Our results using quantitative RT-PCR showed that E(2) increased bcl-2 mRNA levels at 48 h of treatment via a transcriptional mechanism. None of the hormone treatments altered the proapoptotic protein levels, bax and bak. We also studied the in vivo expression of bcl-2 and other members of its family in biopsies of normal breast tissues according to the menstrual cycle. Bcl-2 displayed a strong cyclical variation and seemed to be the most hormone-dependent member of the family.
Steroids
PMID:Hormonal regulation of apoptosis in breast cells and tissues. 1110 64

Radiation induced lung injury has long been considered a treatment limiting factor for patients requiring thoracic radiation. This radiation induced lung injury happens early as well as late. Radiation induced lung injury can occur in two phases viz. early (<6 months) when it is called radiation pneumonitis and late (>6 months) when it is called radiation induced lung fibrosis. There are multiple factors that can be patient, disease or treatment related that predict the incidence and severity of radiation pneumonitis. Radiation induced damage to the type I pneumocytes is the triggering factor to initiate such reactions. Over the years, radiation therapy has witnessed a paradigm shift in radiation planning and delivery and successfully reduced the incidence of lung injury. Radiation pneumonitis is usually a diagnosis of exclusion. Steroids, ACE inhibitors and pentoxyphylline constitute the cornerstone of therapy. Radiation induced lung fibrosis is another challenging aspect. The pathophysiology of radiation fibrosis includes continuing inflammation and microvascular changes due to pro-angiogenic and pro- fibrogenic stimuli resembling those in adult bronchiectasis. General supportive management, mobilization of airway secretions, anti-inflammatory therapy and management of acute exacerbations remains the treatment option. Radiation induced lung injury is an inevitable accompaniment of thoracic radiation.
Asian Pac J Cancer Prev 2015
PMID:Radiation induced lung injury: prediction, assessment and management. 2585 36

The etiologies of optic neuropathy include inflammation, ischemia, toxic and metabolic injury, genetic disease, and trauma. There is little controversy over the practice of using steroids in the treatment of optic neuritis--it is well established that intravenous steroid treatment can speed visual recovery but does not alter final visual function. However, there is controversy surrounding the acceptable routes of administration, dosage, and course of treatment. Additionally, the typical patient with optic neuritis is young and otherwise healthy, and thus is likely to tolerate steroids well. In ischemic and traumatic causes of optic neuropathies, the initial injury is not inflammatory, but damage may be compounded by secondary injury due to resultant inflammation and swelling in the confined space of the optic canal. Steroids have been considered as a means of minimizing inflammation and swelling, and thus minimizing the secondary injury that results. However, the use of steroids in traumatic and ischemic optic neuropathies is highly controversial-the evidence for the efficacy of treatment with steroids is insufficient to show that there is significant benefit. Additionally, patients with these conditions are more likely to have comorbidities that make them vulnerable to significant adverse events with the use of steroids. In this article, we attempt to analyze the current state of the literature regarding the use of steroids in the treatment of optic neuropathies, specifically optic neuritis, nonarteritic anterior ischemic optic neuropathy, and traumatic optic neuropathy.
Asia Pac J Ophthalmol (Phila)
PMID:Steroid Treatment of Optic Neuropathies. 2996 19