Detection of the complex of chromatin DNase-tRNA by gel filtration

By gel filtration on Sephadex G-100, the formation of the complex of chromatin DNase-tRNA has been detected. The complex is reactivated after RNase treatment. The molecular weight of the enzyme-inhibitory complex is estimated to be 85,000.     

Effect of hydrocortisone on the level and metabolism of phospholipids in the rat cerebral cortex

Hydrocortisone was studied for its effect in vivo and in vitro on the phospholipids content and metabolism in the rat brain slices under conditions of their incubation in the medium with [2-14C]acetate. The seven-day administration of the preparation increases the specific radioactivity of sphingomyelin 2 times and that of phosphatidyl serine 2.3 times. The quantity of phosphatidic acid after the single administration of hydrocortisone decreases almost twice and its specific radioactivity (1 mg per 100 g of mass) increases two times. Under conditions of the preparation action in vitro the specific radioactivity of phosphatidyl inositol increases on the average five times. The 10(-4) M concentration of hydrocortisone in the medium makes the quantity of phosphatidic acid 1.4 times lower and the specific radioactivity of phosphatidyl-ethanol amine 1.9 times lower. Results of the study are discussed as related to the role of phospholipids in the processes of ionic transport and regulation of the genome activity.     

Deficit of glucocorticoid production in rats aggravates ulcerogenic effects of stimuli of various modality and intensity

Effects of glucocorticoid deficiency and corticosterone replacement on gastric mucosal injury induced by various ulcerogenic stimuli have been evaluated in rats. Gastric erosions were induced in male rats by stimuli of different modalities and intensities. Glucocorticoid deficiency was induced by adrenalectomy or delayed inhibitory action after a single pharmacological dose of cortisol (300 mg/kg, i.p.) injected one week before the onset of ulcerogenic stimulus. Ulcerogenic stimuli induced both a plasma corticosterone rise and a gastric mucosal injury. The area of mucosal damages induced various stimuli ranging from a small to extensive those. Glucocorticoid deficiency significantly potentiated an ulcerogenic action of each ulcerogenic stimulus. Replacement by corticosterone (4 mg/kg, s.c., 15 min before the onset of ulcerogenic stimulus) prevented or significantly decreased the erosion--potentiating effect of glucocorticoid deficiency. These results show that endogenous glucocorticoids released during ulcerogenic influences help gastric mucous membrane to resist against a harmful action of both weak and strong ulcerogenic stimuli.     

Central corticotropin-releasing factor (CRF) may attenuate somatic pain sensitivity through involvement of glucocorticoids

Corticotropin-releasing factor (CRF) is an important regulator of physiological functions and behavior in stress. Analgesia is one of the characteristics of stress reaction and CRF is involved in providing stress-induced analgesia, however, the underlying mechanisms remain to be determined. Exogenous CRF mimics stress effects on pain sensitivity and causes analgesic effect. The present study was performed to investigate the participation of endogenous glucocorticoids in analgesic effects induced by central administration of CRF in anesthetized rats. The participation of glucocorticoids was studied by pharmacological suppression of the hypothalamic-pituitary-adrenocortical (HPA) axis as well as an occupation of glucocorticoid receptors by its antagonist RU 38486. Since CRF administration causes the release of β-endorphin from the pituitary, the opioid antagonist naltrexone was used to determine the contribution of opioid-dependent mechanism to CRF-induced analgesia. An electrical current threshold test was applied for measurement of somatic pain sensitivity in anesthetized rats. Intracerebroventricular administration of CRF (2 μg/rat) caused analgesic effects (an increase of pain thresholds) and an increase in plasma corticosterone levels. Pretreatment with naltrexone did not change analgesic effects of central CRF as well as corticosterone levels in blood plasma. However, pharmacological suppression of the HPA axis leading to an inability of corticosterone release in response to CRF resulted in an elimination of CRF-induced analgesic effects. Pretreatment with RU 38486 also resulted in an elimination of CRF-induced effects. The data suggest that CRF-induced analgesic effects may be mediated by nonopioid mechanism associated with endogenous glucocorticoids released in response to central CRF administration.     

Long non‐coding RNAs in melanoma

Melanoma is the most lethal cutaneous cancer with a highly aggressive and metastatic phenotype. While recent genetic and epigenetic studies have shed new insights into the mechanism of melanoma development, the involvement of regulatory non‐coding RNAs remain unclear. Long non‐coding RNAs (lncRNAs) are a group of endogenous non‐protein‐coding RNAs with the capacity to regulate gene expression at multiple levels. Recent evidences have shown that lncRNAs can regulate many cellular processes, such as cell proliferation, differentiation, migration and invasion. In the melanoma, deregulation of a number of lncRNAs, such as HOTAIR, MALAT1, BANCR, ANRIL, SPRY‐IT1 and SAMMSON, have been reported. Our review summarizes the functional role of lncRNAs in melanoma and their potential clinical application for diagnosis, prognostication and treatment.