We have seen substantial changes in minimally invasive surgery since its development in the early 1900s. Over the past 10 years, the addition of natural orifice transluminal endoscopic surgery and robotics has turned our attention to improved cosmesis and advancements in instrumentation. We have developed a new technique-single port access (SPA) surgery-and have applied it to the cholecystectomy. In this paper, we present and review the application of this access technique to the first 5 consecutive patients that underwent an SPA cholecystectomy. All 5 patients were female, with an average age of 45 years and an average weight of 172 pounds. Indications included biliary dyskinesia and symptomatic cholelithiasis. Average operative time was 121 minutes in these initial 5 cases. All but 1 patient was discharged in 24 hours. At 6 months, no umbilical hernias were observed. This new technique allows for a complete cholecystectomy to be performed entirely through the umbilicus without the need for additional retraction sites or transabdominal sutures. This procedure utilizes the same basic technique of the laparoscopic cholecystectomy already employed by general surgeons. Therefore, the SPA cholecystectomy can be readily learned and performed by many surgeons without the need for expensive or experimental equipment. Using a single portal of entry to the abdominal cavity, the umbilicus, cosmesis, and scar reduction is achieved.

Intrapulmonary engraftment of engineered lung tissues could provide a potential therapeutic approach for the treatment of pediatric and adult pulmonary diseases. In working toward this goal, we report here on in vivo generation of vascularized pulmonary tissue constructs utilizing the subcutaneous Matrigel plug model. Mixed populations of murine fetal pulmonary cells (FPCs) containing epithelial, mesenchymal, and endothelial cells (ECs) were isolated from the lungs of embryonic day 17.5 fetuses. FPCs were admixed to Matrigel and injected subcutaneously into the anterior abdominal wall of adult C57/BL6 mice to facilitate in vivo pulmonary tissue construct formation. Vascularization was enhanced by placing fibroblast growth factor 2 (FGF2)-loaded polyvinyl sponges into the hydrogel. After 1 week, routine histology and immunohistochemical staining for donor-derived epithelial cells and ECs as well as analysis of patent vasculature in the constructs following tail vein injection of fluorescein isothiocyanate-conjugated dextran were performed. In the Matrigel-only controls, some level of host infiltrate, but no measurable vascularization, was detected. In the presence of FPCs, the constructs contained ductal epithelial structures and patent vasculature. In the absence of FPCs, exogenous FGF2 induced the formation of numerous patent blood vessels throughout the entire constructs; in combination with FPCs, it resulted in enhanced capillary density and abundant interfacing between developing epithelial and vascular structures. The significant findings of this study are that distal pulmonary epithelial differentiation (as assessed by the expression of prosurfactant protein C) can be maintained in vivo and that donor-derived ECs contribute to the formation of patent vessels that interface tightly with ductal epithelial structures.

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Free fatty acids (FFAs), including arachidonic acid (AA), are implicated in the direct and indirect modulation of a spectrum of voltage-gated ion channels. Skeletal muscle sodium channels can be either activated or inhibited by FFA exposure; the response is dependent on both FFA structure and site of exposure. Recombinant human skeletal muscle sodium channels (hSkM1) were transfected into heterologous human renal epithelium HEK293t cells. Cytoplasmic delivery of 5 M AA augmented the voltage-activated sodium current of hSkM1 channels by 190% (؎54 S.E., n ‫؍‬ 7) over a 20-min period. Similar results were seen with 5 M oleic acid. Sodium currents in HEK293t cells transfected with human cardiac muscle sodium channels (hH1) were insensitive to AA treatment, and exposure to oleic acid inhibited the hH1 currents over a 20-min period by 29% (؎13 S.E., n ‫؍‬ 5). The increase in hSkM1 current was not accompanied by shifts in voltage dependence of activation, steady-state inactivation, or markedly altered kinetics of inactivation of the macroscopic current. The FFA-induced increase in sodium currents was not dependent on protein kinase C activity. In contrast, both isoforms were reversibly inhibited by external application of unsaturated FFA. Thus, the differential effects of FFA on skeletal muscle sodium channels first noted in cultured muscle cells can be reproduced by expressing recombinant sodium channels in epithelial cells. Although the responses to applied FFAs could be direct or indirect, we suggest that: 1) SkM1 has two classes of response to FFA, one which produces augmentation of macroscopic currents with intracellular FFA, and a second which produces inhibition with extracellular FFA; 2) H1 has only one class of response, which produces inhibition with extracellular FFA. A testable hypothesis is that the presence or absence of each response is due to a specific structure in SkM1 or H1. These specific structures may directly interact with FFA or may interact with intermediate components.

Increased iliac calcification and increased iliac tortuosity correlate with an inability to successfully deploy the device.