Kinaesthetic Sensitivity Of Normal And Clumsy Children

Laszlo and Bairstow (1985a) stated that their Kinaesthetic Sensitivity Test (KST) was designed to be useful in researching the relationship between kinaesthesis and motor performance, and as a diagnostic tool to identify children with poor kinaesthetic function. This study examined the claim that many clumsy children perform poorly on the KST. It was found that the test failed to distinguish between the performances of clumsy children and those of an age-matched control group. Because of its psychometric shortcomings, the KST is unable to fulfil the claims of Laszlo and Bairstow, either as a research or a clinical tool.     

The liver in infectious mononucleosis

Summary 1. Twenty-two patients with infectious mononucleosis were studied by liver biopsy and paper electrophoresis of the serum proteins. The findings were compared with a similar group of 30 patients with infectious hepatitis.2. The essential histologic features of infectious mononucleosis were the presence in the hepatic sinusoids and portal tracts of chronic inflammatory cells resembling small lymphocytes, with essentially no parenchymal cell damage. Admixed with this lymphocytic infiltrate, but in relatively minimal numbers, were a few plasma cells and polymorphonuclear leukocytes. In addition, in infectious mononucleosis there were, with rare exceptions, no lipochrome-containing Kupffer cells. Thus, in the majority of cases, the histologic picture was distinct from that seen in infectious hepatitis. Only in comparing a few of the more severe infectious mononucleosis cases with subsiding infectious hepatitis cases was there any tendency for the two pictures to merge, and the distinction on histologic grounds between the two entities could be made in the great majority of cases.3. The most commonly seen abnormalities in the paper electrophoretic patterns of sera obtained from patients with infectious mononucleosis were decreased albumin, increased gamma globulin, not infrequent but variable changes in alpha₂ globulin, and the presence of abnormal proteins migrating with mobilities intermediate to alpha₂ and beta, and beta and gamma globulins. The abnormalities observed in infectious hepatitis were similar to those of infectious mononucleosis, except that in hepatitis alpha₂ globulin was decreased more consistently, gamma globulin increased less frequently, and beta globulin, which was normal in practically all the cases of infectious mononucleosis, was increased in a considerable number of cases.4. Treatment of patients with infectious mononucleosis need not include prolonged bed rest and restriction of activity in an effort to avoid the development of chronic liver disease.     

Cause-effect relation between hyperfibrinogenemia and vascular disease

Elevated plasma levels of fibrinogen are associated with the presence of cardiovascular disease, but it is controversial whether elevated fibrinogen causally imparts an increased risk, and as such is a true modifier of cardiovascular disease, or is merely associated with disease. By investigating a transgenic mouse model of hyperfibrinogenemia, we show that elevated plasma fibrinogen concentration (1) elicits augmented fibrin deposition in specific organs, (2) interacts with an independent modifier of hemostatic activity to regulate fibrin turnover/deposition, (3) exacerbates neointimal hyperplasia in an experimental model of stasis-induced vascular remodeling, yet (4) may suppress thrombin generation in response to a procoagulant challenge. These findings provide direct experimental evidence that hyperfibrinogenemia is more than a by-product of cardiovascular disease and may function independently or interactively to modulate the severity and/or progression of vascular disease.     

The cartilage matrix molecule components produced by human foetal cartilage rudiment cells within scaffolds and the role of exogenous growth factors

Development of cartilage lesions in osteoarthritis and following traumatic injury has important consequences on the weight bearing and articulation of joints, has severe impact on the quality of life of affected individuals and is of significant socioeconomic impact. Hyaline cartilage is a highly specialised tissue with a limited ability to self repair. Development of three-dimensional scaffolds which maintain the correct chondrocyte phenotype during expansion of cells in vitro and their application in regenerative strategies for cartilage repair is therefore a major research objective of many laboratories. This study examined the matrix components elaborated by cultured foetal cartilage rudiment cells, a mixture of chondroblasts/chondroprogenitor cells and committed chondrocytes, in monolayer, cell pellet cultures and in the synthetic scaffolds sodium alginate and polyglycolic acid (PGA). The ability of fibroblast growth factor (FGF)-2 and FGF-18 to promote chondrogenesis in pellet cultures was also examined. While the scaffolds did not completely replicate the matrix organisation evident in native cartilage, type II collagen and aggrecan were nevertheless prominent matrix components. FGF-2 and FGF-18 further promoted the production of cartilage-specific matrix components in pellet culture as FGF-18 stimulated the production of type X collagen and perlecan and may be indicative of a more terminally differentiated phenotype induced in the rudiment cells with this growth factor.     

Infection with Anaplasma phagocytophilum activates the phosphatidylinositol 3-Kinase/Akt and NF-κB survival pathways in neutrophil granulocytes

Anaplasma phagocytophilum, a Gram-negative, obligate intracellular bacterium infects primarily neutrophil granulocytes. Infection with A. phagocytophilum leads to inhibition of neutrophil apoptosis and consequently contributes to the longevity of the host cells. Previous studies demonstrated that the infection inhibits the executionary apoptotic machinery in neutrophils. However, little attempt has been made to explore which survival signals are modulated by the pathogen. The aim of the present study was to clarify whether the phosphatidylinositol 3-kinase (PI3K)/Akt and NF-κB signaling pathways, which are considered as important survival pathways in neutrophils, are involved in A. phagocytophilum-induced apoptosis delay. Our data show that infection of neutrophils with A. phagocytophilum activates the PI3K/Akt pathway and suggest that this pathway, which in turn maintains the expression of the antiapoptotic protein Mcl-1, contributes to the infection-induced apoptosis delay. In addition, the PI3K/Akt pathway is involved in the activation of NF-κB in A. phagocytophilum-infected neutrophils. Activation of NF-κB leads to the release of interleukin-8 (IL-8) from infected neutrophils, which, in an autocrine manner, delays neutrophil apoptosis. In addition, enhanced expression of the antiapoptotic protein cIAP2 was observed in A. phagocytophilum-infected neutrophils. Taken together, the data indicate that upstream of the apoptotic cascade, signaling via the PI3K/Akt pathway plays a major role for apoptosis delay in A. phagocytophilum-infected neutrophils.     

Ultrastructural identification of cells with dendritic cell appearance in atherosclerotic aorta of apolipoprotein E deficient mice

The present electron microscopic study was undertaken to see whether cells with a dendritic cell appearance accumulate in atherosclerotic lesions of apolipoprotein E (apoE) deficient mice. Atherosclerotic aortas from 7 eight-month old apoE deficient mice were examined. In atherosclerotic plaques as well as in the underlying media and adventitia, cells with a dendritic cell appearance including the presence of a unique tubulovesicular system were detected. The tubulovesicular system was most hypertrophied in their cellular processes where the continuous cisterns sometimes formed circular structures. The cells containing the tubulovesicular system lacked lysosomes and phagolysosomes and their cytoplasm was free of lipid inclusions. The present observations suggest that dendritic cells are involved in apoE deficient mouse atherosclerosis. ApoE deficient mice might be a useful model for investigating functions of dendritic cells in atherogenesis.     

Sources of Error in the Estimation of Mosquito Infection Rates Used to Assess Risk of Arbovirus Transmission

Infection rate is an estimate of the prevalence of arbovirus infection in a mosquito population. It is assumed that when infection rate increases, the risk of arbovirus transmission to humans and animals also increases. We examined some of the factors that can invalidate this assumption. First, we used a model to illustrate how the proportion of mosquitoes capable of virus transmission, or infectious, is not a constant fraction of the number of infected mosquitoes. Thus, infection rate is not always a straightforward indicator of risk. Second, we used a model that simulated the process of mosquito sampling, pooling, and virus testing and found that mosquito infection rates commonly underestimate the prevalence of arbovirus infection in a mosquito population. Infection rate should always be used in conjunction with other surveillance indicators (mosquito population size, age structure, weather) and historical baseline data when assessing the risk of arbovirus transmission.