Cholinesterase in larvae of the ascidian,Ciona intestinalis,developing from fragments cut from centrifuged eggs

Development Genes and Evolution - UnfertilizedCiona eggs were centrifuged, stratifying their mitochondria and some other cytoplasmic components. Each centrifuged egg had a mitochondria-free,...     

Relationship between inspiratory effort and breathlessness in pregnancy.

Using open-magnitude scaling, we compared the relationships between breathlessness, inspiratory esophageal pressure swing (delta Pes), and ventilation in pregnancy and postpartum. Thirteen healthy women performed progressive cycle exercise tests at 33 +/- 2 wk gestation and 12 +/- 3 wk postpartum. Pulmonary function and maximal transdiaphragmatic pressure did not change. Minute ventilation (VE) was greater in the third trimester. This increase was entirely due to the increase in tidal volume (VT; 0.74 +/- 0.18 vs. 0.54 +/- 0.18 liters at rest, P less than 0.01; 1.56 +/- 0.3 vs. 1.24 +/- 0.24 liters at 48 W, P less than 0.001). delta Pes (15.3 +/- 3.0 vs. 11.9 +/- 3.5 cmH2O at 48 W, P less than 0.01) and breathlessness (1.8 +/- 1.4 vs. 1.0 +/- 0.9 at 48 W, P less than 0.05) were greater in the third trimester. However, the relationships between VT and delta Pes and between delta Pes and breathlessness were identical in the two conditions. The VT-tidal abdominal volume (Vab) and Vab-tidal gastric pressure swing (delta Pga) relationships were similar in the two conditions. In conclusion, the relationship between delta Pes and breathlessness is the same in the third trimester and postpartum. The increased VE is responsible for the breathlessness in the third trimester. Despite progressive abdominal distension by the gravid uterus, the VT-Vab and Vab-delta Pga relationships were the same in the two conditions.     

Genetic and physical mapping of a novel region close to the fragile X site on the human X chromosome

We report the isolation and characterization of a novel DNA marker (1A1) in Xqter in the region of the fragile X. Genetic studies in families segregating for the fragile X syndrome suggest that 1A1 lies between the disease mutation and the distal locus, DXS52. Studies in normal and fragile X families show that 1A1 is tightly linked to DXS52 (Zmax = 17.20; theta max = 0.03) and F8 (Zmax = 7.01; theta max = 0.08). Multipoint mapping of families supports the order Xcen-DXS105-FRAXA-1A1-DXS52-(F8, DXS115)-Xqter. Pulsed-field gel electrophoresis (PFGE) studies demonstrate that 1A1 defines a new region of at least 2 Mb of DNA not physically linked to DXS52 or F8, thus extending the physical map of Xq27-qter to over 4 Mb. Complex partial digestion PFGE patterns, probably due to differing degrees of methylation, are observed with 1A1 in unrelated normal and fragile-X-positive individuals, whereas other distal markers give uniform digestion profiles. Physical data suggest that 1A1 lies in a region less CpG rich than other distal markers in Xq27-qter.