Incision length correlates with patient weight, height, and gender when using a minimal-incision technique in total hip arthroplasty.

Minimal-incision technique in total hip arthroplasty (THA) has been previously defined as requiring an incision of 10 cm or less. A higher complication rate for overweight or muscular patients has been demonstrated when this arbitrary cutoff is used. The purpose of this study was to perform minimal-incision technique surgery without a specific incision length cutoff on a cohort of nonselected, consecutive THA patients to determine if patient height, weight, body mass index, gender, type of femoral fixation, and/or age correlated with incision length. A total of 115 patients underwent THA (posterior approach) using minimal-incision technique by a single, experienced surgeon who performed the smallest incision that was feasible. There was a significant correlation between incision size and patient weight (p < .0001)), height (p = .007), and gender (p = .04). Complications included one patient each with postoperative instability, an intraoperative calcar fracture, and an intraoperative distal incision skin tear. These findings demonstrate that larger patients can expect a longer incision with this technique, and that for a given weight, women will have longer incisions than men. Selecting appropriate incision length for minimally invasive THA reduces potential associated complications.

Fine mapping of a major QTL influencing morphine preference in C57BL/6 and DBA/2 mice using congenic strains.

C57BL/6J (B6) and DBA/2J (D2) mice differ in behaviors related to substance abuse, including voluntary morphine consumption and preference in a two-bottle choice paradigm. Two major quantitative trait loci (QTL) for morphine consumption and preference exist between these strains on chromosomes (Chrs.) 6 and 10 when the two-bottle choice involves morphine in saccharin vs quinine in saccharin. Here, we report the refinement of the Chr. 10 QTL in subcongenic strains of D2.B6-Mop2 congenic mice described previously. With these subcongenic mouse strains, we have divided the introgressed region of Chr. 10 containing the QTL gene(s) into two segments, one between the acromere and Stxbp5 (in D2.B6-Mop2-P1 mice) and the other between marker D10Mit211 and marker D10Mit51 (in D2.B6-Mop2-D1 mice). We find that, similar to B6 mice, the D2.B6-Mop2-P1 congenic mice exhibit a strong preference for morphine over quinine, whereas D2.B6-Mop2-D1 congenic mice avoid morphine (similar to D2 mice). We have also created a line of double congenic mice, B6.D2-Mop2.Qui, which contains both Chr. 10 and Chr. 6 QTL. We find that they are intermediate in their morphine preference scores when compared with B6 and D2 animals. Overall, these data suggest that the gene(s) involved in morphine preference in the morphine-quinine two-bottle choice paradigm are contained within the proximal region of Chr. 10 (which harbors Oprm1) between the acromere and Stxbp5, as well as on distal Chr. 6 between marker D6Mit10 and the telomere.

Synthesis and calculated properties of some 1,4-bis(amino)anthracene-9,10-diones.

The synthesis of a number of 1,4-bis(amino)anthracene-9,10-diones containing chlorine or sulfur which are related to the anti-cancer drugs Ametantrone and Mitoxantrone are reported. 1,4-Dichloro-2,3-dihydro-5,8-dihydroxyanthracene-9,10-dione reacts readily with a series of alkylamines to yield the corresponding 1,4-bis(alkylamino)-5,8-dichloroanthracene-9,10-dione after oxidation. The subsequent reaction of the products with ethanethiol or thiophenol gives the corresponding 1,4-bis(alkylamino)-5,8-bis(sulfanyl)anthracene-9,10-dione in good yield. Theoretical calculations at the RHF 6-31G** level indicate that the introduction of either chlorine or the phenylsulfanyl group into the 5- and 8-positions of 1,4-bis(alkylamino)anthracene-9,10-diones results in a lowering of the LUMO energies suggesting that related functionalised derivatives might have lower cardiotoxicities than Mitoxantrone.

AKT activation and response to interferon-beta in human cancer cells.

Significant growth inhibition and induction of apoptosis by IFN-beta in cancer cells including colorectal cancer cells have been observed. We and others have previously reported the Stat 1 induction of TRAIL is a crucial step in the IFN-beta induced apoptosis pathway. However, when evaluating the sensitivity of a panel of colorectal cancer cell lines, we found no clear correlation between activation of the Jak/Stat signaling pathway and response to interferon. In the present study, we have evaluated the interaction of the PI3k/Akt pathway and IFN-beta induced apoptosis in human colorectal cancer cells. The results demonstrate a correlation between Akt activity, phosphorylation of Bad and resistance to interferon-induced apoptosis in these cells. The association of activation of Akt, phosphorylation of Bad and resistance to IFN-beta-induced apoptosis was further supported by the observation that disruption of the pathway in a more resistant cell line led to sensitization, and expression of an activated Akt in a more sensitive cell line led to increased resistance. Taken together, this data indicates that the PI3/Akt kinase pathway may be an important contributor to IFN-beta sensitivity and resistance in colorectal cancer cells. This data demonstrates a potential pathway by which cells may develop resistance to IFN, and further elucidation of this process may allow us to better target IFN therapy.