Bee Venom Induces Unfolded Protein Response in A172 Glioblastoma Cell Line

Background: Glioblastoma is a type of brain tumor with poor response to available therapies, and shows high rate of mortality. Despite remarkable advancements in our knowledge about cytogenetic and pathophysiologic features of glioblastoma, current treatment strategies are mainly based on cytotoxic drugs; however, these therapeutic approaches are facing progressive failure because of the resistant nature of glioblastomas. In the recent years, however, promising results have emerged owing to targeted therapies toward molecular pathways within cancerous cells. Unfolded Protein Response (UPR) is a remarkable signaling pathway that triggers both apoptosis and survival pathways within cells, and therefore induces UPR-related apoptotic pathways in cancer cells by ER stress inducers. Objectives: Recently, the role of Bee venom (Bv), which contains powerful bioactive peptides, in inducing UPR-related apoptosis was revealed in cancer cell lines. Nevertheless, currently there are no reports of Bv potential ability in induction of UPR apoptotic routes in glioblastoma. The aim of current study was to evaluate possible role of Bee venome in inducing of UPR pathway within A172 glioblastoma cell line. Materials and Methods: We treated the A172 glioblastoma cell line with different Bv doses, and assessed UPR-related genes expression by real-time Polymerase Chain Reaction (PCR). Results: The IC50 of Bv for the studied cell line was 28 μg/mL. Furthermore, we observed that Bv can induce UPR target genes (Grp94 and Gadd153) over-expression through a dose-dependent mechanism. Conclusions: Our results suggest the potential role of Bv as a therapeutic agent for glioblastomas. Keywords: Glioblastoma; A172 Cell Line; Unfolded Protein Response; Bee Veno

Persistence of back pain symptoms after pregnancy and bone mineral density changes as measured by quantitative ultrasound - a two year longitudinal follow up study

<p>Abstract</p> <p>Background</p> <p>Previous research has shown a loss of bone mineral density (BMD) during pregnancy. This loss has been correlated to the occurrence of back pain symptoms during pregnancy. The objective of this study was to evaluate whether persistence of back pain symptoms 2 years after pregnancy could be associated with BMD changes as measured by quantitative USG of the os calcis.</p> <p>Methods</p> <p>A cohort of patients who reported significant back pain symptoms during pregnancy were surveyed for persistent back pain symptoms 24 to 28 months after the index pregnancy. Os calcis BMD was measured by quantitative ultrasound and compared with the BMD values during pregnancy.</p> <p>Results</p> <p>A cohort of 60 women who had reported significant back pain symptoms in their index pregnancy completed a 24-28 months follow-up survey and BMD reassessment. Persistence of significant back pain symptoms was seen in 24 (40%) of this cohort. These women had higher BMD loss during pregnancy compared to those without further pain (0.047 Vs 0.030 g/cm²; p = 0.03). Those that remained pain free after pregnancy appeared to have completely recovered their BMD loss in pregnancy, while those with persistent pain had lower BMD values (ΔBMD - 0.007 Vs - 0.025 g/cm²; p = 0.023) compared to their early pregnancy values.</p> <p>Conclusion</p> <p>Persistence of back pain symptoms after pregnancy could be related to an inability to recover fully from BMD loss during the index pregnancy.</p

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Age at onset of multiple sclerosis is correlated to use of combined oral contraceptives and childbirth before diagnosi

Running title: Prevention of menstrual migraine

Prevention of menstrual migraine with perimenstrual transdermal 17-beta-estradiol: a randomized, placebo-controlled, double-blind crossove

Perinatal and Family Risk Factors for Hodgkin Lymphoma in Childhood Through Young Adulthood

The incidence of Hodgkin lymphoma has increased among adolescents and young adults in recent decades, but the relevant risk factors in early life are still unknown. A national cohort study was conducted of 3,571,574 individuals born in Sweden in 19732008 and followed up for Hodgkin lymphoma incidence through 2009, to examine perinatal and family risk factors for Hodgkin lymphoma in childhood through young adulthood (ages 037 years). There were 943 Hodgkin lymphoma cases identified in 66.3 million person-years of follow-up. High fetal growth was associated with an increased risk of Hodgkin lymphoma after adjustment for gestational age at birth and other potential confounders (P-trend 0.005). Family history of Hodgkin lymphoma in a sibling or parent also was strongly associated with an increased risk, with adjusted hazard ratios 8.83 (95 confidence interval: 3.67, 21.30) and 7.19 (95 confidence interval: 3.58, 14.44), respectively. No association was found between gestational age at birth, birth order, twinning, parental age, or parental education and Hodgkin lymphoma. These findings did not vary by age at Hodgkin lymphoma diagnosis. Similar associations were found for nodular sclerosis and mixed cellularity subtypes. These findings suggest that perinatal factors including possible growth factor pathways may contribute to the risk of Hodgkin lymphoma in childhood through young adulthood