Scanner-Based Protocol-Driven Ultrasound: An Effective Method to Improve Efficiency in an Ultrasound Department.

OBJECTIVE: For ultrasound, a wide variation is often observed among the number and sequence of images acquired for a particular examination type. Scanner-based protocols are preset pathways in the ultrasound machine that guide a sonographer through the required study images. These protocols can streamline image acquisition by improving consistency and efficiency of ultrasound examinations. This study evaluated whether implementation of scanner-based protocol-driven ultrasound improves efficiency by decreasing the scanning duration and number of images acquired. MATERIALS AND METHODS: Retrospective evaluation of 437 carotid Doppler examinations, 395 complete abdominal ultrasound examinations with Doppler imaging, and 413 bilateral lower extremity venous Doppler examinations for deep venous thrombosis (DVT) performed by five sonographers before and after implementation of scanner-based protocol-driven ultrasound was performed. The scanning duration and number of images acquired for each study were recorded. Statistical analysis compared the scanning duration and number of images acquired before and after implementation of protocol-driven ultrasound. A p value of < 0.05 was considered significant. RESULTS: A significant decrease in scanning duration occurred for both carotid Doppler ultrasound examinations (decrease by 12.4% [2.7 minutes], p < 0.0001) and complete abdominal ultrasound examinations with Doppler imaging (decrease by 7.5% [2.0 minutes], p = 0.0054) after implementation of protocol-driven ultrasound. The decrease in scanning duration was not significant for lower extremity DVT Doppler examinations (p = 0.4192). In addition, there was a significant decrease in the overall number of images obtained for all three types of studies. CONCLUSION: Scanner-based protocol-driven ultrasound is an effective method that streamlines image acquisition and significantly improves efficiency in an ultrasound department while ensuring consistency and adherence to accreditation guidelines.

Effect of Anticoagulation Medication on the Thyroid Fine-Needle Aspiration Pathologic Diagnostic Sufficiency Rate.

OBJECTIVES: This study examined whether ultrasound-guided thyroid fine-needle aspiration (FNA) biopsy performed on patients taking anticoagulation medication results in a greater number of nondiagnostic pathologic samples due to a higher propensity to bleed, and thus fill the needle with blood rather than cellular material, compared to patients not taking anticoagulation medication. METHODS: In this retrospective review, data were collected on 1100 patients who underwent ultrasound-guided thyroid FNA over a 4-year period. Of these patients, 438 were included. Each thyroid FNA was performed by a board-certified radiologist using a 6-pass capillary fill technique. Data including patient age, sex, nodule size, nodule consistency, and whether the patient was or was not taking anticoagulation medication (and, if they were, which medication) were recorded from the electronic medical record, and the nodule characteristics were confirmed on imaging by a senior radiology resident (postgraduate year 5). RESULTS: Of the 438 patients included, 12 (2.7%) had an FNA aspirate that was deemed insufficient for diagnostic evaluation. Nondiagnostic pathologic yields were seen in 7 of the 309 patients (2.3%) who were not taking anticoagulation medication and 5 of 129 patients (3.9%) who were taking aspirin, warfarin, or clopidogrel, resulting in no statistically significant difference in the rates of nondiagnostic pathologic yields between the two groups (P = .35). CONCLUSIONS: Based on these data, cessation of anticoagulation medication before thyroid FNA is not necessary to obtain sufficient cellular material for diagnosis, thus eliminating the need for procedural delays, patient inconvenience, and risks associated with anticoagulation medication cessation.

Transepithelial elimination in sarcoidosis: a frequent finding.

BACKGROUND: Transepithelial elimination is a process by which dermal materials are expelled through an active epithelial-dermal connective tissue interaction. It has been described as a regular or sporadic occurrence in a variety of dermatologic conditions, including sarcoidosis. OBSERVATION: Our patient demonstrated a rare presentation of sarcoidosis involving the genital region, with histopathologic evidence of transepithelial elimination of granulomas. This prompted us to conduct the first case series documenting the frequency of transepithelial elimination in sarcoidosis. METHODS: Slides of skin biopsies from patients (n = 50) with cutaneous sarcoidosis from the University of Alabama at Birmingham were evaluated for transepithelial elimination. Transepithelial elimination was defined as epithelial channel formation with a sarcoidal-type granuloma completely surrounded by squamous epithelium on the section examined. RESULTS: Transepithelial elimination was found in 9 of 50 cases (18%). CONCLUSION: This is the first report of transepithelial elimination in a lesion of sarcoidosis localized to the vulvar area, and one of only six reports in the English literature documenting cutaneous sarcoidosis with histopathologic evidence of transepithelial elimination. These reports are reviewed herein. Surprisingly, the results from this case series indicate that transepithelial elimination is more common in cutaneous sarcoidosis than one may surmise from the current literature.

Pre-osteoblastic MC3T3-E1 cells promote breast cancer growth in bone in a murine xenograft model.

The bones are the most common sites of breast cancer metastasis. Upon arrival within the bone microenvironment, breast cancer cells coordinate the activities of stromal cells, resulting in an increase in osteoclast activity and bone matrix degradation. In late stages of bone metastasis, breast cancer cells induce apoptosis in osteoblasts, which further exacerbates bone loss. However, in early stages, breast cancer cells induce osteoblasts to secrete inflammatory cytokines purported to drive tumor progression. To more thoroughly evaluate the role of osteoblasts in early stages of breast cancer metastasis to the bones, we used green fluorescent protein-labeled human breast cancer cell lines MDA-MB-231 and MDA-MB-435, which both induce osteolysis after intra-femoral injection in athymic mice, and the murine pre-osteoblastic cell line MC3T3-E1 to modulate osteoblast populations at the sites of breast cancer metastasis. Breast cancer cells were injected directly into the femur with or without equal numbers of MC3T3-E1 cells. Tumors grew significantly larger when co-injected with breast cancer cells and MC3T3-E1 cells than injected with breast cancer cells alone. Osteolysis was induced in both groups, indicating that MC3T3-E1 cells did not block the ability of breast cancer cells to cause bone destruction. MC3T3-E1 cells promoted tumor growth out of the bone into the extraosseous stroma. These data suggest that breast cancer cells and osteoblasts communicate during early stages of bone metastasis and promote tumor growth.

Type I interferons: key players in normal skin and select cutaneous malignancies.

Interferons (IFNs) are a family of naturally existing glycoproteins known for their antiviral activity and their ability to influence the behavior of normal and transformed cell types. Type I Interferons include IFN- α and IFN- ß . Currently, IFN- α has numerous approved antitumor applications, including malignant melanoma, in which IFN- α has been shown to increase relapse free survival. Moreover, IFN- α has been successfully used in the intralesional treatment of cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC). In spite of these promising clinical results; however, there exists a paucity of knowledge on the precise anti-tumor action of IFN- α / ß at the cellular and molecular levels in cutaneous malignancies such as SCC, BCC, and melanoma. This review summarizes current knowledge on the extent to which Type I IFN influences proliferation, apoptosis, angiogenesis, and immune function in normal skin, cutaneous SCC, BCC, and melanoma.

Subsets of ATP-sensitive potassium channel (KATP) inhibitors increase gap junctional intercellular communication in metastatic cancer cell lines independent of SUR expression.

Gap junctional intercellular communication (GJIC) regulates cellular homeostasis by propagating signaling molecules, exchanging cellular metabolites, and coupling electrical signals. In cancer, cells exhibit altered rates of GJIC which may play a role in neoplastic progression. K(ATP) channels help maintain membrane polarity and linkages between K(ATP) channel activity and rates of GJIC have been established. The mechanistic relationship has not been fully elucidated. We report the effects of treatment with multiple K(ATP) antagonist compounds on GJIC in metastatic cell lines demonstrating an increase in communication rates following treatment with compounds possessing specificities towards the SUR2 subunit of K(ATP). These effects remained consistent using cell lines with different expression levels of SUR1 and SUR2, suggesting possible off target effects on GJIC by these compounds.

Homotypic gap junctional communication associated with metastasis suppression increases with PKA activity and is unaffected by PI3K inhibition.

Loss of gap junctional intercellular communication (GJIC) between cancer cells is a common characteristic of malignant transformation. This communication is mediated by connexin proteins that make up the functional units of gap junctions. Connexins are highly regulated at the protein level and phosphorylation events play a key role in their trafficking and degradation. The metastasis suppressor breast cancer metastasis suppressor 1 (BRMS1) upregulates GJIC and decreases phosphoinositide-3-kinase (PI3K) signaling. On the basis of these observations, we set out to determine whether there was a link between PI3K and GJIC in tumorigenic and metastatic cell lines. Treatment of cells with the well-known PI3K inhibitor LY294002, and its structural analogue LY303511, which does not inhibit PI3K, increased homotypic GJIC; however, we found the effect to be independent of PI3K/AKT inhibition. We show in multiple cancer cell lines of varying metastatic capability that GJIC can be restored without enforced expression of a connexin gene. In addition, while levels of connexin 43 remained unchanged, its relocalization from the cytosol to the plasma membrane was observed. Both LY294002 and LY303511 increased the activity of protein kinase A (PKA). Moreover, PKA blockade by the small molecule inhibitor H89 decreased the LY294002/LY303511-mediated increase in GJIC. Collectively, our findings show a connection between PKA activity and GJIC mediated by PI3K-independent mechanisms of LY294002 and LY303511. Manipulation of these signaling pathways could prove useful for antimetastatic therapy.