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Background Median arcuate ligament syndrome (MALS) is a rare disorder characterized by postprandial abdominal pain, weight loss, and celiac stenosis. Diagnosis can be challenging, leading to a delay in treatment. We report on our continued experience using a laparoscopic approach for this uncommon diagnosis. Methods This is an Institutional Review Board-approved, prospectively collected retrospective analysis of patients treated with laparoscopic MAL release at our institution. Data collected included patient demographics, preoperative symptoms, operative approach, and postoperative outcomes. Patients were then contacted to complete a postoperative survey designed to assess the improvement of symptoms and overall patient satisfaction. Results A total of 39 patients (33 women and 6 men) underwent laparoscopic MAL release from March 2007 to July 2014. Mean age was 40.6 years (range, 17–77 years). Thirty of 39 patients had a postoperative celiac axis ultrasound. Twenty-three had a patent celiac axis on postoperative duplex. Of the remaining 7, 5 with residual celiac axis stenosis and 1 with occlusion, reported complete resolution of their symptoms. One remaining patient with occlusion remained symptomatic. Thirty-three of 39 (84.6%) reported symptom relief after surgery. Nine of 33 (27.3%) responders had cardiovascular risk factors versus 4 of 6 (67%) nonresponders. Five patients with atypical presentations underwent preoperative diagnostic celiac plexus block using local anesthetic, with 4 reporting symptom reliefs after block. These 4 patients also reported postoperative symptom relief. One patient of 39 received a postoperative celiac stent placement and remained symptomatic. There were 4 conversions to open surgery (10.3%) and no deaths. Conclusions Laparoscopic MAL release continues to be a safe and effective means of managing MALS. Our data suggest that the symptoms associated with MALS are not related to vascular compromise, and atherosclerotic risk factors may predict poorer outcomes. Symptomatic relief is seen in the vast majority of patients undergoing this procedure. However, patient selection remains critically important in obtaining optimal results.

An accurate diagnosis is essential for making treatment decisions in dentistry. However, little research is available as to which tests are done routinely and how commonly they are performed. The purpose of this study was to investigate diagnostic methods and equipment used by general dentists in private practice in Perth. The study involved a retrospective audit of 30 patient records from seven individual general dentists working in private practices in the Perth Metropolitan area. De-identification of patient records was done prior to the researchers' visit. Radiographs were the most commonly used diagnostic tool. Percussion was also commonly employed, followed by cold pulp testing and mobility. The most commonly used tests were radiographs, percussion, periodontal probing and visual examination. The frequency of these tests differed depending on whether the patient presented with or without pain, with percussion and cold tests used more frequently when the patient presented with pain.

Though gastrointestinal (GI) hemorrhage is common, it can be a life-threatening condition. There are numerous etiologies for GI bleeding, and these are often grouped according to location in the GI tract. With the increasing use of endoscopy for diagnosis of GI bleeding, the development of endoscopic hemostatic techniques has followed. Injection therapy, electrocautery, and hemostatic clips were some of the early hemostatic modalities available for use. Today, the number of available endoscopic hemostatic devices has grown to include band ligation, sclerotherapy, over-the-scope clips, and full thickness suturing techniques. This chapter examines the etiologies of upper, lower, and obscure GI bleeding, and presents techniques to manage GI hemorrhage through the endoscope.

Examination of the hip provides information regarding risk for pre-arthritic hip disorders, knee injuries, and low back pain. The purpose of this study was to report a hip screening examination of asymptomatic female soccer athletes and to test the hypothesis that these findings vary by competition experience.Asymptomatic females from a youth soccer club, a college, and a professional team were evaluated. Passive hip range of motion, hip abduction strength, and hip provocative tests were assessed. Data were compared for the grade/middle school, high school, college, and professional athletes.One hundred and seventy-two athletes with a mean age of 16.7 ± 5 years (range 10-30) participated. Professional athletes had less flexion (HF) for both hips (p0.0001) and less internal rotation (IR) for the preferred kicking leg (p0.05) compared to all other groups. Grade/middle school athletes had more external rotation in both hips as compared to all other groups (p0.0001). For the preferred kicking leg, collegiate athletes had less hip abduction strength as compared to other groups (p0.01). Positive provocative hip tests were found in 22 % of all players and 36 % of the professionals. In professionals, a positive provocative test was associated with ipsilateral decreased HF (p = 0.04).Asymptomatic elite female soccer athletes with the most competition experience had less bilateral hip flexion and preferred kicking leg IR than less-experienced athletes. Positive provocative hip tests were found in 22 % of athletes. Future studies are needed to show whether these findings link to risk for intra-articular hip or lumbar spine and knee disorders.III.

The authors would like to provide a clarification in relation to Figure 1 in the article. Although all the cell lines/lanes were exposed together (see accompanying original raw blots), most site panels were not run in adjacent lanes but were cut and pasted to fit the figure format. We provide a revised Figure 1 where a dividing vertical line indicates which lanes were not adjacent in the raw blot. Furthermore, the bands for the breast cancer panel are slightly overcropped and a band for the CNS panel (present in the original raw blot) was cut off. In part, this is due to the fact that cell line SF295 was ran together with the positive control lung cell line H-520 (see figure 2) that is not a member of the NIH-60 cell panel and was cropped out from the original raw blot to fit the description of this figure dedicated to the NCI-60 cell panel. Raw Blots: (1) Figure 1

VILIP-1, a member of the neuronal Ca(2+) sensor protein family, is able to act as a tumor suppressor in carcinoma cells by inhibiting cell proliferation and migration. In order to study the role of VILIP-1 in skin carcinogenesis we generated transgenic mice overexpressing VILIP-1 in epidermis under the control of the bovine keratin K5 promoter (K5-VILIP-1). We studied the susceptibility of FVB wild type and VILIP-1 transgenic mice to chemically mediated carcinogenesis. After 30 weeks of treatment with a two-stage carcinogenesis protocol, all animals showed numerous skin tumors. Nevertheless, K5-VILIP-1 mice showed decreased squamous cell carcinoma (SCC) multiplicity of approximately 49% (p

VILIP-1, a member of the neuronal Ca++ sensor protein family, acts as a tumor suppressor gene in an experimental animal model by inhibiting cell proliferation, adhesion and invasiveness of squamous cell carcinoma cells. Western Blot analysis of human tumor cells showed that VILIP-1 expression was undetectable in several types of human tumor cells, including 11 out of 12 non-small cell lung carcinoma (NSCLC) cell lines. The down-regulation of VILIP-1 was due to loss of VILIP-1 mRNA transcripts. Rearrangements, large gene deletions or mutations were not found. Hypermethylation of the VILIP-1 promoter played an important role in gene silencing. In most VILIP-1-silent cells the VILIP-1 promoter was methylated. In vitro methylation of the VILIP-1 promoter reduced its activity in a promoter-reporter assay. Transcriptional activity of endogenous VILIP-1 promoter was recovered by treatment with 5′-aza-2′-deoxycytidine (5′-Aza-dC). Trichostatin A (TSA), a histone deacetylase inhibitor, potently induced VILIP-1 expression, indicating that histone deacetylation is an additional mechanism of VILIP-1 silencing. TSA increased histone H3 and H4 acetylation in the region of the VILIP-1 promoter. Furthermore, statistical analysis of expression and promoter methylation (n = 150 primary NSCLC samples) showed a significant relationship between promoter methylation and protein expression downregulation as well as between survival and decreased or absent VILIP-1 expression in lung cancer tissues (p