Academic advancement of authors receiving tutoring from a medical journal

BACKGROUND: Although publishing in scientific journals has an educational component, the educational role of journals in medicine has not been evaluated. - - - - - PURPOSE: To assess whether tutoring authors in a medical scientific journal could be related to their long-term scientific publications and academic advancement. - - - - - METHODS: The study included 47 journal authors who were individually tutored in scientific writing and data presentation by the editors of the Croatian Medical Journal during the 1991-1995 war years and 47 colleagues the authors identified as their academic peers at the time of tutoring. We assessed their published articles in scientific journals, citations to these articles, and academic advancement, defined as the level of postgraduate education and advancement in the academic rank. - - - - - RESULTS: By 2003, tutored authors published more articles in MEDLINE-indexed journals than their academic peers (median = 4, interquartile range = 1-9 vs. 1 [0-5], respectively; p = .0265), and received more citations to these articles (4 [0-16] vs. 1 [0-6], p = .0275). They also made a significantly greater academic advancement, assessed as a score of their academic rank and research degree (2 [0-4] vs. 1 [0-2], p = .0369). - - - - - CONCLUSIONS: Editorial tutoring of journal authors can positively influence their long-term academic advancement. Journals may have an important teaching role in local academic communities

Fas receptor is required for estrogen deficiency-induced bone loss in mice

Bone mass is determined by bone cell differentiation, activity, and death, which mainly occur through apoptosis. Apoptosis can be triggered by death receptor Fas (CD95), expressed on osteoblasts and osteoclasts and may be regulated by estrogen. We have previously shown that signaling through Fas inhibits osteoblast differentiation. In this study we analyzed Fas as a possible mediator of bone loss induced by estrogen withdrawal. At 4 weeks after ovariectomy (OVX), Fas gene expression was greater in osteoblasts and lower in osteoclasts in ovariectomized C57BL/6J (wild type (wt)) mice compared with sham-operated animals. OVX was unable to induce bone loss in mice with a gene knockout for Fas (Fas -/- mice). The number of osteoclasts increased in wt mice after OVX, whereas it remained unchanged in Fas -/- mice. OVX induced greater stimulation of osteoblastogenesis in Fas -/- than in wt mice, with higher expression of osteoblast-specific genes. Direct effects on bone cell differentiation and apoptosis in vivo were confirmed in vitro, in which addition of estradiol decreased Fas expression and partially abrogated the apoptotic and differentiation-inhibitory effect of Fas in osteoblast lineage cells, while having no effect on Fas-induced apoptosis in osteoclast lineage cells. In conclusion, the Fas receptor has an important role in the pathogenesis of postmenopausal osteoporosis by mediating apoptosis and inhibiting differentiation of osteoblast lineage cells. Modulation of Fas effects on bone cells may be used as a therapeutic target in the treatment of osteoresorptive disorders