Ethanol induces hyperprolactinemia by increasing prolactin release and lactotrope growth in female rats

BACKGROUND: Alcohol drinking is known to cause hyperprolactinemia in both humans and laboratory animals. The mechanism by which alcoholism causes hyperprolactinemia is not known. This study investigated whether increased pituitary production of prolactin, which leads to alcohol-induced hyperprolactinemia, results from an increase in cell number and/or cell production of prolactin in the pituitary. METHODS: The effects of ethanol on lactotropes were determined in vivo using female rats as an animal model and in vitro using primary cultures of mixed rat anterior pituitary cells and enriched lactotropes. In vivo experiments involved administration of ethanol for 2 and 4 weeks using a liquid diet containing 8.7% ethanol (v/v), which provides 37% of the calories in cyclic, ovariectomized, and estradiol-17beta-treated ovariectomized Fischer-344 rats. The control group was pair-fed an isocaloric diet minus the ethanol or fed a normal diet ad libitum. These animals were used to determine ethanol's effects on plasma prolactin levels, pituitary wet weights, pituitary total protein levels, and the number of mitotic lactotropes. In vitro studies determined ethanol's effects in the presence and absence of estradiol on prolactin release and lactotropic cell proliferation. Prolactin levels in plasma and media samples were measured using radioimmunoassay. Mitotic lactotropes were determined using bromodeoxyuridine incorporation assay. RESULTS: Ethanol treatment increased in a time-dependent manner the plasma levels of prolactin in cyclic, ovariectomized, and estradiol-treated ovariectomized rats. Ethanol treatment also increased pituitary wet weight and/or pituitary total protein levels and DNA synthesis in lactotropes. Determination of ethanol's action on lactotropic cell proliferation and hormone secretion in vitro using primary cultures of mixed pituitary cells revealed that ethanol stimulated both basal and estradiol-induced prolactin secretion and lactotropic cell proliferation. When ethanol's actions were studied in isolated lactotropes, ethanol alone or in combination with estradiol stimulated prolactin secretion but failed to increase lactotropic cell proliferation. CONCLUSIONS: These results suggest that ethanol causes hyperprolactinemia by elevating prolactin release from lactotropes and by increasing the number of lactotropes in the anterior pituitary gland. The mitotic action of ethanol requires cell-cell communication between lactotropes and other pituitary cells. Furthermore, ethanol's mode of action on prolactin release and lactotrope growth is similar to that observed for estradiol.     

Detection of HBsAg in newborns

Cord blood samples collected from 150 newborns were tested for HBsAg using micro ELISA technique. Only 8 (5.3 per cent) out of 150 samples were found to be positive for HBsAg in variable titres. It is important to identify these HBsAg positive newborns so that appropriate measures could be adopted at the earliest to prevent the complications of HBsAg carriage.     

Histological observations on the anterior olfactory nucleus in human

Aim: Localization of isolated clusters of anterior olfactory nucleus (AON) in a human olfactory bulb and tract. Materials and methods: This investigation was done on human olfactory bulbs and their tracts, collected from the freshly donated cadavers, before embalming, in the Department of Anatomy, IPGMER, Kolkata. H&E stained histological slides were prepared along the whole length of specimens and examined under a Leica DM 2000 microscope and with a Leica Quin image analyzer. Results: The anterior olfactory nucleus was detected in the form of a major cluster and in two smaller clusters of neurons. The major cluster was located at the caudal pole of the bulb and was composed of medium-sized triangular cells which had an average diameter of 13.92 ± 3.43 μm. Out of the two minor clusters, one was detected at the beginning and another at the middle of the olfactory tract. Here neurons were little larger in size and their diameter ranged approximately 15–17 μm. Olfactory striae also accommodated some neurons in a scattered manner. Conclusion: This observation will be helpful in exploration of the complex role of AON in the organization and function of the olfactory system and its clinical significance in human.     

Pediatric maxillofacial injuries and its management

BackgroundPediatric facial injuries are common due to children's high level of activity which gradually decreases as age advances. Main etiology in cases of pediatric age group are self-fall, sports related injuries, interpersonal violence and lastly road traffic accident. Pattern and management of facial fracture in pediatric age group is different to that of adult population.Material and methodsThis study included 87 patients who had facial injuries and who reported at dental institute RIMS, Ranchi over a period of three years from 2017 to 2020. Initial assessment diagnosis and management were given to the patients.ResultsSelf-fall accounted as the leading cause of fracture (47.1%). Most frequent age group with facial injuries were from 7 to 12 years age group (49.1%). Dentoalveolar pattern of facial fracture was most common accounting for (39.1%) followed by mandible fracture in 33.3%. Closed reduction of the fracture was the most common way of treatment. Open reduction and fixation was carried out in 3.4% patients.ConclusionSelf-fall was the main etiology in our study and younger age group patients were more involved. Conservative treatment are generally given to pediatric age group, with open reduction in few cases on the basis of displacement. Close monitoring and follow up is mandatory in these age group.