31 research outputs found
Competence acquisition for single-incision laparoscopic cholecystectomy
BACKGROUND AND OBJECTIVES: Within the past few years, there has been a push for an even more minimally invasive approach to biliary disease with the adoption of single-incision laparoscopic cholecystectomy. We sought to compare 4 individual surgeon experiences to define whether there exists a learning curve for performing single-incision laparoscopic cholecystectomy. METHODS: We performed a retrospective review 290 single-incision laparoscopic cholecystectomies performed by a group of general surgeons, with varying levels of experience and training, at 3 institutions between May 2008 and September 2010. The procedure times were recorded for each single-incision laparoscopic cholecystectomy, ordered chronologically for each surgeon, and subsequently plotted on a graph. The patients were also combined into cohorts of 5 and 10 cases to further evaluate for signs of improvement in operative efficiency. RESULTS: Of the 4 surgeons involved in the study, only 1 (surgeon 4, laparoscopic fellowship trained with \u3c5 \u3eyears\u27 experience) confirmed the presence of a learning curve, reaching proficiency within the first 15 cases performed. The other surgeons had more variable procedure times, which did not show a distinct trend. When we evaluated the cases by cohorts of 5 cases, surgeon 4 had a significant difference between the first and last cohort. Increased body mass index resulted in a slightly longer operative time (P \u3c .0063). The conversion rate to multiport laparoscopic surgery was 3.1%. CONCLUSIONS: Our results indicate that among experienced general surgeons, there does not seem to be a significant learning curve when transitioning from conventional laparoscopic cholecystectomy to single-incision laparoscopic cholecystectomy. The least experienced surgeon in the group, surgeon 4, appeared to reach proficiency after 15 cases. Greater than 5 years of experience in laparoscopic surgery appears to provide surgeons with a sufficient skill set to obviate the need for a single-incision laparoscopic cholecystectomy learning curve
Identification of a nuclear protein binding element within the rat brain protein kinase C Îł promoter that is related to the developmental control of this gene
Growth Hormone Deficiency and Splicing Fidelity: TWO SERINE/ARGININE-RICH PROTEINS, ASF/SF2 AND SC35, ACT ANTAGONISTICALLY*
The majority of mutations that cause isolated growth hormone deficiency
type II are the result of aberrant splicing of transcripts encoding human
growth hormone. Such mutations increase skipping of exon 3 and encode a
17.5-kDa protein that acts as a dominant negative to block secretion of
full-length protein produced from unaffected alleles. Previously, we
identified a splicing regulatory element in exon 3 (exonic splicing enhancer 2
(ESE2)), but we had not determined the molecular mechanism by which this
element prevents exon skipping. Here, we show that two members of the
serine/arginine-rich (SR) protein superfamily (ASF/SF2 and SC35) act
antagonistically to regulate exon 3 splicing. ASF/SF2 activates exon 3
inclusion, but SC35, acting through a region just downstream of ESE2, can
block such activation. These findings explain the disease-causing mechanism of
a patient mutation in ESE2 that creates a functional SC35-binding site that
then acts synergistically with the downstream SC35 site to produce
pathological levels of exon 3 skipping. Although the precedent for SR proteins
acting as repressors is established, this is the first example of a patient
mutation that creates a site through which an SR protein represses
splicing