Activated platelets release various growth factors, some of which are recognized to improve nerve regeneration. This study evaluated the effect of platelet-rich plasma (PRP) in end-to-end neurorrhaphy. A total of 45 Wistar rats were used, with the initial five used for PRP preparation. The right hind limbs were used as experimental, with the left as control. The animals were treated in five groups. Group A (n = 4): The right sciatic nerve was dissected only from the sciatic notch to the bifurcation. In all other groups, the nerve was sharply transected and repaired with: group B (n = 8): two sutures; group C (n = 8): six sutures; group D (n = 10): two sutures and PRP; and group E (n = 10): six sutures and PRP. Groups D and E were compared with groups B and C, respectively. Group E had a shorter latency time in electromyography ( P < 0.01) and a thicker myelin layer in the histological evaluation ( P < 0.003) in comparison with group C. These positive effects of PRP were not detected in the nerves were repaired with two sutures. In this animal model, the application of PRP to the repair site helped to improve remyelinization of the sciatic nerve in rats when the epineural repair was done with six sutures.

Iron-refractory iron-deficiency anemia (IRIDA) is a rare autosomal-recessive disorder characterized by hypochromic microcytic anemia, low transferrin saturation, and inappropriate high levels of the iron hormone hepcidin. The disease is caused by variants in the transmembrane protease serine 6 (TMPRSS6) gene that encodes the type II serine protease matriptase-2, a negative regulator of hepcidin transcription. Sequencing analysis of the TMPRSS6 gene in 21 new IRIDA patients from 16 families with different ethnic origin reveal 17 novel mutations, including the most frequent mutation in Southern Italy (p.W590R). Eight missense mutations were analyzed in vitro. All but the p.T287N variant impair matriptase-2 autoproteotylic activation, decrease the ability to cleave membrane HJV and inhibit the HJV-dependent hepcidin activation. Genotype-phenotype studies in IRIDA patients have been so far limited due to the relatively low number of described patients. Our genotype-phenotype correlation analysis demonstrates that patients carrying two nonsense mutations present a more severe anemia and microcytosis and higher hepcidin levels than the other patients. We confirm that TMPRSS6 mutations are spread along the gene and that mechanistically they fully or partially abrogate hepcidin inhibition. Genotyping IRIDA patients help in predicting IRIDA severity and may be useful for predicting response to iron treatment.

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Our study suggests that hepcidin levels do not contribute to the development of iron deficiency anemia in pediatric obese individuals.

Idiopathic thrombocytopenic purpura (ITP) in children is usually a self-limiting disorder. It may follow a viral infection or immunization and is caused by an inappropriate response of the immune system. Many viruses, such as human immunodeficiency virus, cytomegalovirus (CMV), Epstein-Barr virus (EBV), varicella, rubeola, mumps, and parvovirus, have been implicated in childhood ITP. This study is a retrospective chart review of pediatric patients diagnosed with virus-associated ITP at the Hacettepe University, Ihsan Dogramaci Children's Hospital from 1997 to end of 2000. In viral serological studies, the EBV, CMV, and rubella antibodies were investigated for all patients at diagnosis (ELlSA). The proportion of children whose ITP was associated with documented acute viral infection was 13.3% in this group. In the present study, clinical manifestations and laboratory data of virus-associated or not associated groups are similar except age. Median age of the virus-associated group is younger than that of the other, but it is not statistically significant.