In this letter we show that it is possible to drastically change electric double layer capacitance, from a large increase to complete disappearance, by introducing various surface functional groups on carbon nanotubes. The introduction of surface carboxyl groups created a 3.2 times larger capacitance due to the increased hydrophilicity of the multiwalled carbon nanotubes in an aqueous electrolyte. In contrast, the introduction of alkyl groups resulted in a marked decrease of capacitance. Notably, we unexpectedly observed the complete disappearance of capacitance for samples functionalized with longer alkyl groups than octyl, indicating the perfect block of proton access to the carbon nanotubes’ surfaces by extreme hydrophobicity.
The chromosomal translocation t(7; 11)(p15;p15), observed in human myeloid leukemia, results in a NUP98 and HOXA9 gene fusion. We generated a transgenic mouse line that specifically expressed the chimeric NUP98-HOXA9 gene in the myeloid lineage. While only 20% of the transgenic mice progressed to leukemia after a latency period, myeloid progenitor cells from nonleukemic transgenic mice still exhibited increased proliferative potential. This suggested that the NUP98-HOXA9 fusion induced a preleukemic phase, and other factors were required for complete leukemogenesis. NUP98-HOXA9 expression promoted the onset of retrovirus-induced BXH2 myeloid leukemia. This phenomenon was used to identify cooperative disease genes as common integration sites (CISs). Meis1, a known HOX cofactor, was identified as a CIS with a higher integration frequency in transgenic than in wild-type BXH2 mice. By the same means we identified further 4 candidate cooperative genes, Dnalc4, Fcgr2b, Fcrl, and Con1. These genes cooperated with NUP98-HOXA9 in transforming NIH 3T3 cells. The system described here is a powerful tool to identify cooperative oncogenes and will assist in the clarification of the multistep process of carcinogenesis. (Blood. 2005;105: 784-793)
Background The direct anterior approach in THA requires no detachment of muscle insertions. However, damage to the short external rotator muscles may occur when attempting to elevate the femur for exposure. Although the anatomic insertions of these muscles are approximately known, there are no quantitative data regarding their locations. Questions/purposes We therefore asked where and how the tendons attach to the inner aspect of the greater trochanter. Methods In 20 cadaveric hips we identified the attachments of the short external rotator tendons on the medial aspect of the greater trochanter. Mapping of the attachment site was performed by defining coordinate axes; the total width and height of the greater trochanter represented 100% and distances of the attachment from the anteroinferior reference point were given.
ResultsThe mean anterior border location of the conjoined tendon (obturator internus, gemellus superior, and gemellus inferior) attachment was located at 29% (13 mm from the anteroinferior reference point), its posterior border at 53% (23 mm), its mean superior border at 70% (15 mm), and its mean inferior border at 24% (5 mm). The mean anterior border of the piriformis tendon attachment was located at 57% (25 mm), its mean posterior border at 78% (34 mm), its mean superior border at 64% (17 mm), and its inferior border at 55% (12 mm). There was considerable variation in these attachment sites among individuals. Conclusions The insertion of the conjoined tendon extends to the anterosuperior aspect of the greater trochanter. Together with the considerable variation of the attachment site, external rotator muscles remain at risk of being damaged during the capsular release.
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