Modulation of prolactin release by a 25 KD peptide of human seminal plasma

Prolactin-regulating factor (PRF) of molecular size of 25 kD has been isolated from human seminal plasma. This 25 kD factor inhibits circulating PRL levels in intact adult male rats to the extent of about 48% at dose level of 10 μg. Furthermore, in vitro incubation of pituitary demonstrated that PRF inhibits the release of PRL in the medium. PRF also interferes with the binding of I125 PRL to its receptors in liver, prostate, and spermatozoa. However, I125 PRF itself does not bind to these receptors. PRF seems to modulate PRL release as well as its binding to receptors. A sensitive, specific RIA was developed for PRF. Using the RIA, levels of PRF in seminal plasma were measured. PRF levels were low in vasectomized subjects as compared with controls. A negative correlation was noted with seminal plasma PRF levels and sperm count

Clinical features, laboratory and molecular findings of children with leukocyte adhesion deficiency type-III from a single center in India

Leukocyte adhesion deficiency (LAD) Type-III is caused by homozygous mutations in FERMT3 causing Kindlin-3 deficiency. Here we describe three children with molecularly proven LAD-III presenting with neonatal onset mucocutaneous bleeding, infections and persistent neutrophilic leukocytosis. CD18 and CD11a expression on neutrophils was normal in all three, thus ruling out LAD-I. All three had normal platelet glycoprotein expression. Platelet aggregation studies in P2 showed an abnormality similar to Glanzmann thrombasthenia. This article aims to highlight clinical and laboratory clues to the diagnosis of LAD-III, aiding prompt administration of prophylaxis and curative therapy of haematopoietic stem cell transplant