Lung function development in the first 2 yr of life is independent of allergic diseases by 2 yr

The aim of the study was to assess if lung function at birth predicts lung function at 2 yr and secondly, if lung function development was influenced by the common phenotypes of recurrent bronchial obstruction (rBO) or atopic eczema (AE) by 2 yr. Lung function was assessed at birth (n = 802) and at 2 yr within the prospective birth cohort study 'the Environment and Childhood Asthma Study' in Oslo. The 135 children with lung function measured at birth by tidal flow volume (TFV) loops and passive respiratory mechanics, who were included in a nested case-control study were reinvestigated at 2 yr with clinical examination, TFV loops (n = 90) (mean age 26.6 (3.7 s.d.) months), skin prick test and parental interview. Children were categorized into quartiles (lower, middle two, upper) according to time to peak tidal expiratory flow/total expiratory time (t(PTEF)/t(E)) at birth as well as clinical phenotype based on the presence of rBO and/or AE (ever) by 2 yr. The observed reduction in mean t(PTEF)/t(E) from birth to 2 yr within the quartiles, were not significantly different after controlling for 'regression to the mean'. t(PTEF)/t(E) at birth correlated significantly with t(PTEF)/t(E) at 2 yr, (r = 0.475, p < 0.001). Children with both rBO and AE by 2 yr had significantly lower t(PTEF)/t(E) at 2 yr (p = 0.002) and at birth (p = 0.027), compared with children with no rBO or AE. Clinical phenotype at 2 yr did not influence the change in t(PTEF)/t(E) from birth to 2 yr. This study demonstrates a clear tracking of lung function from birth, not influenced by rBO or AE by 2 yr.     

Free tissue transfer for type III tibial fractures. Microsurgery in 19 cases.

We report 19 tibial fractures Types III B and C treated by free flaps. The fracture healed in 16 cases after 12 (3-54) months. In 3 cases a secondary amputation was carried out. Tibial malalignment or substantial shortening ensued in 1 case each. We conclude that coverage with free flaps, radical removal of dead bone, stable external fixation and transfer of vascularized bone may salvage the majority of Type III B and C tibial fracture with function superior to that after amputation.     

Effects of C5a and FMLP on Interleukin-8 Production and Proliferation of Human Umbilical Vein Endothelial Cells

Interleukin-8 (IL-8), C5a and N-formyl-methionyl-leucyl-phenylalanine (fMLP) are chemotactic peptides with predominant effects on leukocytes during inflammation. With emphasis on C5a we studied the regulation of the production of IL-8 by human umbilical vein endothelial cells (HUVEC) in vitro. Primary HUVEC cultures were incubated with IL-1, TNF, C5a and fMLP for 24 h and 48 h prior to measurement of IL-8 in supernatants of the cells by an enzyme immunoassay. Whereas IL-1 and TNF significantly increased the levels of IL-8, C5a decreased the IL-8 production after 48 h. In addition, the ability of IL-1, TNF, C5a, fMLP and IL-8 to induce cell proliferation was compared by means of a ³H-thymidine incorporation assay. In contrast with IL-1 and TNF, both C5a and fMLP increased cell proliferation of HUVEC. This increase occurred with increasing concentrations of C5a contrary to IL-8, which showed increased cell proliferation at low, but not high IL-8 concentrations.     

Attempts to isolate virus from human trigeminal and facial ganglions

Herpes virus hominis type 1 was isolated from the trigeminal ganglion (ganglion semilunare, gasservian) in three out of 20 randomly selected autopsies. Two of the three patients had been treated with immunosuppressive or cytostatic agents. Clinical signs of herpes infection were not observed during the previous 6 months. No virus was isolated from the facial ganglion (geniculate ganglion) in the same 20 cases. The findings are discussed in relation to the viral etiology of acute peripheral facial palsy.     

Activation of complement during apheresis.

C3 activation products and the terminal complement complex (TCC) were examined in plasma during plasmapheresis of patients with Guillain-Barré Syndrome (GBS) (n = 4), Waldenström''s syndrome (n = 4), and hypercholesterolaemia (n = 1), or during cytapheresis of platelet (n = 10) and granulocyte (n = 2) donors. Blood specimens were taken before, during and after the procedures. There was a significant activation of complement after apheresis in the GBS patients and one of the patients with Waldenström''s syndrome, but not in the other patients. There were no significant differences in complement activation products before compared with after cytapheresis in the healthy donors. This demonstrates the biocompatibility with respect to complement activation of the materials used. The observed complement activation in some of the patients during plasma exchange is probably caused by activation products in the replacement plasma.     

Chemotaxins C5a and fMLP induce release of calprotectin (leucocyte L1 protein) from polymorphonuclear cells in vitro.

AIMS: To determine whether the chemotaxins C5a and formyl peptide (fMLP) can stimulate the release of calprotectin, the major leucocyte protein of polymorphonuclear neutrophils (PMN). METHODS: A dose response curve for the uptake of 125I labelled rC5a and fMLP in PMN was determined by radioimmunoassay. The unlabelled chemotaxins were then incubated with PMN and the concentration of calprotectin in PMN lysates and supernatants was measured by an enzyme immunoassay. RESULTS: Both rC5a and fMLP induced release of calprotectin from PMN in a dose dependent manner as determined by a reduction in intracellular calprotectin concentration. A minimum of approximately 10% of total PMN calprotectin was retained at concentrations of 10-100 nM of rC5a and 0.1-10.0 nM of fMLP. Antibodies to C5a reduced the rC5a mediated release of calprotectin, and the fMLP antagonist N-t-Boc-MLP inhibited the fMLP induced calprotectin release. Because receptors for rC5a (CD88) and fMLP are G protein coupled and thought to be pertussis toxin sensitive, PMN were incubated with this toxin before the experiments. The toxin was found to reduce uptake of rC5a by the cells and to inhibit rC5a and fMLP mediated calprotectin release. CONCLUSIONS: rC5a and fMLP mediate release of calprotectin from PMN in vitro. This effect might be important during human infections in vivo.     

Association between food patterns and difficulties in falling asleep among adolescents in Norway — a descriptive Young-Hunt3 study

Journal of Public Health - Adolescents’ sleep duration has decreased over the past century; this is mainly caused by problems with falling asleep. Short sleep duration, poor sleep quality,...     

Diagnostic and Severity-Tracking Biomarkers for Autism Spectrum Disorder

Autism spectrum disorder (ASD) is a neurodevelopmental disorder afflicting about one in every 68 children. It is behaviorally diagnosed based on a triad of symptoms, including impairment in communication, impairment in sociability and abnormal and stereotypic behavior. The subjectivity of behavioral diagnosis urges the need for clinical biomarker tests to improve and complement ASD diagnosis and treatment. Over the past two decades, researchers garnered a broad range of biomarkers associated with ASD and often correlating with the severity of ASD, which includes metabolic and genetic biomarkers or neuroimaging abnormalities. Metabolic biomarkers are either involved in key pathways such as a trans-sulfuration pathway or produced due to the derangement of these pathways in the case of oxidative stress. Recent studies reported several genetic abnormalities related to ASD, encompassing various mechanisms, from copy number variations (CNVs) and single nucleotide polymorphisms (SNPs) to chromosomal anomalies. However, it is still premature to consider these genetic variants as true biomarkers for ASD, due to their low reproducibility and regional-specific nature. Herein, we comprehensively review state of the art about major biomarkers reported in ASD and the association of some biomarkers with ASD symptoms and severity. It is important to establish those biomarkers to be able to help in the diagnosis and to optimize the treatment of ASD.