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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In each menstrual cycle only very few follicles in the mammalian ovary undergo maturation and ovulation while most of the follicles degenerate in the process of atresia. Moreover, in the absence of pregnancy, the newly formed corpora lutea will degenerate and disappear in the process of luteolysis. Recent studies suggest that ovarian follicular atresia is associated with DNA fragmentation and degeneration of follicular cells, characteristics of programmed cell death (apoptosis). Apoptosis can be induced in vitro, in primary granulosa cell culture, by serum deprivation and by induction of a high intracellular level of cAMP. This induction of apoptosis can be blocked by fibroblast growth factor, suggesting that receptor-medicated activation of a tyrosine kinase can serve as a survival signal. Apoptosis can also be induced in immortalized steroidogenic granulosa cells, transformed by SV40 DNA and Ha-ras oncogene, by overexpression of the wild-type p53 tumor suppressor gene in cAMP-stimulated cells. Omitting the cAMP stimulus prevents the p53-induced apoptosis in these cells, suggesting cross-talk between p53 and c-AMP-generated signals in the induction of apoptosis. Steroidogenic activity in these cells, as well as in nontransformed granulosa cells, does not decline during apoptosis but is rather significantly elevated before total cell collapse occurs. Cytochemical studies using confocal laser microscopy, electron microscopy, and three-dimensional reconstruction reveal a specific reorganization pattern of proteasomes, the most abundant nonlysosomal protease, and of the steroidogenic organelles, such as mitochondria and lipid droplets, in the apoptotic cell. Our results suggest that compartmentalization of intracellular organelles during apoptosis permits proteolysis without interfering with steroidogenesis, characteristic of the differentiated phenotype of the granulosa cell. Moreover, cytoskeletal rearrangement may serve as a barrier between these cellular activities.
Steroids 1996 Apr
PMID:Cross-talk between cAMP and p53-generated signals in induction of differentiation and apoptosis in steroidogenic granulosa cells. 873 10

Ovarian cell death is an essential process for the homeostasis of ovarian function in human and other mammalian species. It ensures the selection of the dominant follicle and the demise of excess follicles. In turn, this process minimizes the possibility of multiple embryo development during pregnancy and assures the development of few, but healthy embryos. Degeneration of the old corpora lutea in each estrous/menstrual cycle by programmed cell death is essential to maintain the normal cyclicity of ovarian steroidogenesis. Although there are multiple pathways that can determine cell death or survival, crosstalk among endocrine, paracrine and autocrine factors, as well as among protooncogenes, tumor suppressor genes, survival genes and death genes, plays an important role in determining the fate of ovarian somatic and germ cells. The establishment of immortalized rat and human steroidogenic granulosa cell lines and the investigation of pure populations of primary granulosa cells allows systematic studies of the mechanisms that control steroidogenesis and apoptosis in granulosa cells. We have discovered that during initial stages of granulosa cell apoptosis progesterone production does not decrease. In contrast, we found that it is elevated up to 24h following the onset of the apoptotic stimuli exerted by starvation, cAMP, p53 or TNF-alpha stimulation, before total cell collapse. These observations raise the possibility for an alternative unique apoptotic pathway, one not involving mitochondrial Cyt C release associated with the destruction of mitochondrial structure and steroidogenic function. Using mRNA from apoptotic cells and affymetrix DNA microarray technology we discovered that granzyme B, a protease that normally resides in T cytotoxic lymphocytes and natural killer cells of the immune system is expressed and activated in granulosa cells. Thus, the apoptotic signals could bypass mitochondrial signals for apoptosis, which can preserve their steroidogenic activity until complete cell destruction. This unique apoptotic pathway assures cyclicity of estradiol and progesterone release in the estrous/menstruous cycle even during the initial stages of apoptosis.
Steroids 2003 Nov
PMID:Steroidogenesis and apoptosis in the mammalian ovary. 1466 78

Aspiration is defined as the inhalation of oropharyngeal or gastric contents into the lower respiratory tract. Upon injury, epithelial cells and alveolar macrophages secrete chemical mediators, attracting and activating neutrophils, which in turn release proteases and reactive oxygen species, degrading the alveolocapillary unit. Aspiration can lead to a range of diseases such as infectious pneumonia, chemical pneumonitis or respiratory distress syndrome with significant morbidity and mortality. It occurs in approximately 3-10 per 10 000 operations with an increased incidence in obstetric and paediatric anaesthesia. Patients are most at risk during induction of anaesthesia and extubation, in particular in emergency situations. The likelihood of significant aspiration can be reduced by fasting, pharmacological intervention and correct anaesthetic management using a rapid sequence induction. Treatment of acid aspiration is by suctioning after witnessed aspiration; antibiotics are indicated in patients with aspiration pneumonia only. Steroids are not proven to improve outcome or reduce mortality. Patients with acute lung injury requiring mechanical ventilation should be ventilated using lung protective strategies with low tidal volumes and low plateau pressure values, attempting to limit peak lung distension and end-expiratory collapse.
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PMID:Bronchoaspiration: incidence, consequences and management. 2115 55

Avascular necrosis of the femoral head is a multifactorial disease with progressive development of severe secondary coxarthrosis. There are two types of necroses - secondary and idiopathic. The pathogenesis of necrosis is associated with local blood circulation disorders, coagulopathies and violation of bone tissue regeneration. Usage of Steroids is one of the most often and important causes of non-traumatic osteonecrosis of the femoral head. Postulated pathogenetic mechanisms of steroid-induced osteonecrosis (ON) of the femoral head includes fat cell hypertrophy, fat emboli and intravascular coagulation. MRI stays the main diagnostic method for detection of osteonecrosis in the early stages. Preservation of the native hip is the goal of treatment in young and active patients. Early diagnosis and intervention prior to collapse of the femoral head is the key to a successful outcome of joint preserving procedures. There are no specific biomarkers for diagnostic of ON and NO "golden standard" for its treatment, and frequently a multidisciplinary approach becomes necessary. Joint replacement procedure remains as a main method of treatment after failure of joint preserving procedures and in cases of the late-stages of ON, involving collapse of the femoral head and degenerative changes of the acetabulum. More recent reports of hip replacement surgeries while osteonecrosis of the femoral head, have shown excellent results, but implant longevity and following revision surgeries, still remain an outstanding problem. In this article, there is described one of the latest clinical cases of the steroid induced avascular necroses of femoral head, which took place in our clinic. Positive clinical outcome, that means full physical and social rehabilitation of the patient, treated by total hip replacement confirms effectiveness of this method in treatment of above mentioned pathology.
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PMID:[STEROID-INDUCED OSTEONECROSES OF FEMORAL HEAD]. 3214 42