Intraoperative arthrography and the Ilizarov technique. Role in the correction of paediatric deformity and leg lengthening

We performed intraoperative arthrography of the knee in 12 children with congenital short femur, Blount's disease or Ollier's disease in whom the Ilizarov technique was used for correction of deformity, leg lengthening or both. In each case, arthrography revealed a joint surface considerably different from that assumed from plain radiographs, and resulted in a change in the placement of our reference wires before application of the frame. This gave significant improvement in the mechanical axis obtained at the time of removal of the frame. The technique is safe, cheap and easy to perform. It is a useful adjunct to the application of the Ilizarov frame when used for complex lengthening and correction of deformity in the leg.     

Changes in selected aspects of immune function in the leopard frog, Rana pipiens, associated with exposure to cold

The effect of exposure to low temperatures (5 degrees C) on lymphocyte proliferation, leukocyte populations, and serum complement levels was examined in the northern leopard frog, Rana pipiens. Proliferation of T lymphocytes in response to phytohemagglutinin stimulation was significantly decreased in frogs kept for 2, 3, and 5 months at 5 degrees C compared to that of animals kept at 22 degrees C. A significant increase in the average percentage of neutrophils and a decrease in the mean percentage of eosinophils was observed in the blood of frogs held for 5 months in the cold compared to animals held at 22 degrees C for the same length of time. Mean serum complement activity after 1 month at 5 degrees C was significantly reduced in comparison to animals held at 22 degrees C and was not detectable after 5 months in the cold. Recovery of complement levels at room temperature (22 degrees C) was also examined after cold exposure. Complement levels were significantly higher than controls (at 22 degrees C) in frogs returned to 22 degrees C for 7 and 14 days after 5 months in the cold. After frogs were held at 5 degrees C for 1 month, serum complement levels increased significantly within 2 days after returning to 22 degrees C and continued to rise 5 and 9 days after warming. Injections with Aeromonas hydrophila following a 5-week exposure to 5 degrees C failed to cause death or observable symptoms of disease in frogs that were returned to 22 degrees C.     

Cellular levels of factor 390 and methanogenic enzymes during growth of Methanobacterium thermoautotrophicum deltaH

Methanobacterium thermoautotrophicum deltaH was grown in a fed-batch fermentor and in a chemostat under a variety of 80% hydrogen-20% CO2 gassing regimes. During growth or after the establishment of steady-state conditions, the cells were analyzed for the content of adenylylated coenzyme F420 (factor F390-A) and other methanogenic cofactors. In addition, cells collected from the chemostat were measured for methyl coenzyme M reductase isoenzyme (MCR I and MCR II) content as well as for specific activities of coenzyme F420-dependent and H2-dependent methylenetetrahydromethanopterin dehydrogenase (F420-MDH and H2-MDH, respectively), total (viologen-reducing) and coenzyme F420-reducing hydrogenase (FRH), factor F390 synthetase, and factor F390 hydrolase. The experiments were performed to investigate how the intracellular F390 concentrations changed with the growth conditions used and how the variations were related to changes in levels of enzymes that are known to be differentially expressed. The levels of factor F390 varied in a way that is consistently understood from the biochemical mechanisms underlying its synthesis and degradation. Moreover, a remarkable correlation was observed between expression levels of MCR I and II, F420-MDH, and H2-MDH and the cellular contents of the factor. These results suggest that factor F390 is a reporter compound for hydrogen limitation and may act as a response regulator of methanogenic metabolism.     

Immunologic characterization of CD7-deficient mice

Human CD7 is an Ig superfamily molecule that is expressed on mature T and NK lymphocytes. Although in vitro studies have suggested a role for CD7 in lymphoid development and function, the exact function of CD7 in vivo has remained elusive. One patient has been reported with SCID syndrome attributed to CD7 deficiency. To study in vivo functions of CD7, we have generated CD7-deficient mice and assessed their lymphoid development and function. CD7-deficient mice were viable, had normal peripheral blood and spleen lymphocyte numbers, and had normal specific Ab responses with Ag-driven Ig isotype switching. Thymocyte numbers were normal in 4-wk-old, 6-mo-old, and 1-yr-old CD7-deficient mice, but in 3-mo-old CD7-deficient mice, total thymocyte numbers were significantly increased by 60% (p < 0.02) compared with normal age-matched +/+ littermates. CD7-deficient splenocytes proliferated normally in response to various mitogens, including PHA, anti-CD3, Con A, and LPS. While NK cell numbers and cytolytic activity to YAC targets were normal, CD7-deficient mice had lower Ag-induced MHC class I-restricted CTL activity against OVA-transfected target cells than did +/+ control mice. Thus, CD7-deficient mice did not have a SCID syndrome, but rather had transient increases in thymocyte numbers at age 3 mo and altered splenocyte Ag-specific CTL effecter cell activity. These data suggest a role for CD7 in regulating intrathymic T cell development and in mediating CTL effecter function.