Association between childhood psychosocial factors and induced abortion

Objective

To examine the predictive associations between psychosocial risk factors in childhood and having an abortion in adolescence or young adulthood.

Study design

This study is based on a nationwide cohort consisting of 2867 girls born in Finland in 1981. The baseline assessment was conducted at age eight by three informants, and it included information on psychiatric symptoms, school performance and family related risk factors. Register-based follow-up data on abortions were collected until the end of the year when the participants turned 28 years. They were available for 2694 participants. Cox proportional hazards model and logistic regression model were used for statistical analysis.

Results

Altogether 357 women (13.3%) had had an abortion for other than medical reasons during the follow-up. Of the childhood factors, a high level of conduct problems, poor school performance, family structure other than two biological parents, and mother with a low level of education were independently associated with having an abortion. Comparison of the strength of associations between childhood risk factors and first abortion under the age of 20 versus first abortion at a later age, showed no significant differences. Neither did the comparison between one and more abortions.

Conclusions

At age eight there are already psychosocial factors which predict later abortion. This finding needs to be considered when targeting preventive interventions and developing sexual health services.     

Lafora progressive myoclonus epilepsy mutation database‐EPM2A and NHLRC1 (EMP2B) genes

Progressive Myoclonus Epilepsy (PME) of the Lafora type is an autosomal recessive disease, which presents in teenage years with myoclonia and generalized seizures leading to death within a decade of onset. It is characterized by pathognomonic inclusions, Lafora bodies (LB), in neurons and other cell types. Two genes causing Lafora disease (LD), EPM2A on chromosome 6q24 and NHLRC1 (EPM2B) on chromosome 6p22.3 have been identified, and our recent results indicate there is at least one other gene causing the disease. The EPM2A gene product, laforin, is a protein tyrosine phosphatase (PTP) with a carbohydrate‐binding domain (CBD) in the N‐terminus. NHLRC1 encodes a protein named malin, containing a zinc finger of the RING type in the N‐terminal half and 6 NHL‐repeat domains in the C‐terminal direction. To date 43 different variations in EPM2A and 23 in NHLRC1 are known, including missense, nonsense, frameshift, and deletions. We have developed a human LD mutation database using a new generic biological database cross‐referencing platform. The database, which currently contains 66 entries is accessible on the World Wide Web ( http://projects.tcag.ca/lafora ). Entries can be submitted via the curator of the database or via a web‐based form. © 2005 Wiley‐Liss, Inc.     

Laminin-5 in the progression of carcinomas.

The basement membrane (BM) separates epithelial elements from the surrounding stroma. BM is dynamic in regulation of epithelial cells differentiation as well as their organization into 3-dimensional tissues. In these functions, among the molecules of the BM, laminins are especially dynamic. Laminins are distributed in a spatially and temporally regulated manner in various epithelial tissues. Various changes in the laminin distribution accompany the malignant transformation of epithelia. The role of the BM and laminins in the progression of carcinomas is not well understood. The BM has been suggested to act as a mechanical barrier against carcinoma cell invasion. BM laminins may play an active role in regulating the migration and proliferation of the carcinoma cells. Laminin isoform laminin-5 expression is typical for some invasive carcinomas and it may act as a ligand for invading carcinoma cells. Neoexpression of laminin-5 has also been associated to proliferative activity of the carcinoma cells. Integrins alpha(3)beta(1) and alpha(6)beta(4) are probable cell surface receptors acting with laminin-5 in the regulation of carcoma cell invasion and proliferation.     

Secretion of celiac disease autoantibodies after in vitro gliadin challenge is dependent on small-bowel mucosal transglutaminase 2-specific IgA deposits

Background

Sand fly saliva contains potent and complex pharmacologic molecules that are able to modulate the host's hemostatic, inflammatory, and immune systems. In this study, we evaluated the effects of salivary gland sonicate (SGS) ofLutzomyia intermedia, the natural vector ofLeishmania braziliensis, on monocytes obtained from the peripheral blood mononuclear cells (PBMC) of healthy volunteers. We investigated the effects of sand fly saliva on cytokine production and surface molecule expression of LPS-stimulated human monocytes uninfected or infected withL. braziliensis.

Results

Pre-treatment of non-infected human monocytes withL. intermediaSGS followed by LPS-stimulation led to a significant decrease in IL-10 production accompanied by a significant increase in CD86, CD80, and HLA-DR expression. Pre-treatment with SGS followed by LPS stimulation andL. braziliensisinfection led to a significant increase in TNF-α, IL-6, and IL-8 production without significant alterations in co-stimulatory molecule expression. However, pre-treatment withL. intermediaSGS did not result in significant changes in the infection rate of human monocytes.

Conclusion

Our data indicate thatL. intermediasaliva is able to modulate monocyte response, and, although this modulation is dissociated from enhanced infection withL. braziliensis, it may be associated with successful parasitism.     

Sacred disease secrets revealed: the genetics of human epilepsy

Neurons throughout the brain suddenly discharging synchronously and recurrently cause primarily generalized seizures. Discharges localized awhile in one part of the brain cause focal-onset seizures. A genetically determined generalized hyperexcitability had been predicted in primarily generalized seizures, but surprisingly the first epilepsy gene discovered, CHRNA4, was in a focal (frontal lobe)-onset syndrome. Another surprise with CHRNA4 was its encoding of an ion channel present throughout the brain. The reason why CHRNA4 causes focal-onset seizures is unknown. Recently, the second focal (temporal lobe)-onset epilepsy gene, LGI1 (unknown function), was discovered. CHRNA4 led the way to mutation identifications in 15 ion channel genes, most causing primarily generalized epilepsies. Potassium channel mutations cause benign familial neonatal convulsions. Sodium channel mutations cause generalized epilepsy with febrile seizures plus or, if more severe, severe myoclonic epilepsy of infancy. Chloride and calcium channel mutations are found in rare families with the common syndromes childhood absence epilepsy and juvenile myoclonic epilepsy (JME). Mutations in the EFHC1 gene (unknown function) occur in other rare JME families, and yet in other families, associations are present between JME (or other generalized epilepsies) and single nucleotide polymorphisms in the BRD2 gene (unknown function) and the malic enzyme 2 (ME2) gene. Hippocrates predicted the genetic nature of the 'sacred' disease. Genes underlying the 'malevolent' forces seizing 1% of humans have now been revealed. These, however, still account for a mere fraction of the genetic contribution to epilepsy. Exciting years are ahead, in which the genetics of this extremely common, and debilitating, neurological disorder will be solved.