The Imaging Features of Desmoid Tumors: the Usefulness of Diffusion Weighted Imaging to Differentiate between Desmoid and Malignant Soft Tissue Tumors

PURPOSE: To evaluate the imaging findings of desmoid tumors using various imaging modalities and to evaluate whether diffusion-weighted imaging (DWI) can help differentiate between desmoid and malignant tumors. MATERIALS AND METHODS: The study included 27 patients with pathologically confirmed desmoid tumors. Two radiologists reviewed 23 computed tomography (CT), 12 magnetic resonance imaging (MRI) and 8 positron emission tomography-computed tomography (PET-CT) scans of desmoid tumors and recorded data regarding the shape, multiplicity, size, location, degree of enhancement, and presence or absence of calcification or hemorrhage. The signal intensity of masses on T1- and T2-weighted imaging and the presence or absence of whirling or band-like low signal intensity on T2-weighted imaging were recorded. The apparent diffusion coefficient (ADC) values of the desmoid tumors in nine patients with DWIs were compared with the ADC values of 32 malignant tumors. The maximum standardized uptake value (SUV(max)) on PET-CT images was measured in 8 patients who underwent a PET-CT. RESULTS: The mean size of the 27 tumors was 6.77 cm (range, 2.5-26 cm) and four tumors exhibited multiplicity. The desmoid tumors were classified by shape as either mass forming (n = 18), infiltrative (n = 4), or combined (n = 5). The location of the tumors was either intra-abdominal (n = 15), within the abdominal wall (n = 8) or extra-abdominal (n = 4). Among the 27 tumors, 21 showed moderate to marked enhancement and 22 showed homogeneous enhancement. Two tumors showed calcifications and one displayed hemorrhage. Eleven of the 12 MR T2-weighted images showed whirling or band-like low signal intensity areas in the mass. The mean ADC value of the desmoid tumors (1493 × 10⁻⁶ mm²/s) was significantly higher than the mean of the malignant soft tissue tumors (873 × 10⁻⁶ mm²/s, P < 0.001). On the PET-CT images, all tumors exhibited an intermediate SUV(max) (mean, 3.7; range, 2.3–4.5). CONCLUSION: Desmoids tumors showed homogenous, moderate to marked enhancement on CT and MRI scans and a characteristic whirling or band-like pattern on T2-weighted images. DWI can be useful for the differentiation of desmoid tumors from malignant soft tissue tumors.

The current epidemiological status of infectious coryza and efficacy of PoulShot Coryza in specific pathogen-free chickens

Infectious coryza (IC) is an infectious disease caused by Avibacterium (Av.) paragallinarum. IC is known to cause economic losses in the poultry industry via decreased egg production in layers. Between 2012 and 2013, Av. paragallinarum was isolated from seven chicken farms by Chungbuk National University. We identified Av. paragallinarum, the causative pathogen of IC by polymerase chain reaction (PCR) and serovar serotype A, by multiplex PCR. Antibiotic sensitivity tests indicated that a few field-isolated strains showed susceptibility to erythromycin, gentamicin, lincomycin, neomycin, oxytetracycline, spectinomycin, and tylosin. A serological survey was conducted to evaluate the number of flocks that were positive for Av. paragallinarum by utilizing a HI test to determine the existence of serovar A. Serological surveys revealed high positivity rates of 86.4% in 2009, 78.9% in 2010, 70.0% in 2011, and 69.6% in 2012. We also challenged specific pathogen-free chickens with isolated domestic strains, ADL121286 and ADL121500, according to the measured efficacy of the commercial IC vaccine, PoulShot Coryza. We confirmed the effectiveness of the vaccine based on relief of clinical signs and a decreased re-isolation rate of ADL121500 strain. Our results indicate IC is currently prevalent in Korea, and that the commercial vaccine is effective at protecting against field strains.

Eggshell apex abnormalities associated with Mycoplasma synoviae infection in layers

Eggs exhibiting eggshell apex abnormalities (EAA) were evaluated for changes in shell characteristics such as strength, thickness, and ultrastructure. Mycoplasma synoviae (MS) infection was confirmed by serological assay along with isolation of MS from the trachea and oviduct. Changes in eggshell quality were shown to be statistically significant (p < 0.01). We also identified ultrastructural changes in the mammillary knob layer by Scanning Electron Microscopy. While eggs may seem to be structurally sound, ultrastructural evaluation showed that affected eggs do not regain their former quality. In our knowledge, this is the first report describing the occurrence of EAA in Korea.

The mechanism of cell death in etoposide treated cervical cancer cells: apoptotic and non-apoptotic programmed cell death / 부인종양

OBJECTIVE: Etoposide is a potent and widely used antineoplastic agent. It is able to induce apoptosis in most cell types. However, very little is known about its mechanism of action. In this study, we demonstrate the cytotoxic signal that induced by etoposide and investigate how etoposide exerts antitumor activity in HPV-16 (+) CaSki cervical carcinoma cells. METHODS: Antiproliferation activity was measured in CaSki cell lines by using MTT assays, DNA fragmentation assay. Cell cycle distribution was analyzed using flow cytometry. Expression of proteins involved in the apoptotic pathway was analyzed by Western blotting (WB). Electron microscopic (EM) and biochemical studies (Western blotting, RT-PCR) revealed that non-apoptotic death was associated with autophagosomes/-autolysosomes. These parameters have also been measured in cells treated with 3-methyladenine (an autophagy inhibitor), zVAD-fmk (a pan-caspase inhibitor) and both. RESULTS: The etoposide induced apoptosis. In cell cycle analysis, etoposide-treated CaSki cells were few induced hypodiploid DNA content, suggesting that apoptotic cell death. EM study revealed that autophagic appearance in the presence of etoposide exhibited by autophagosomes/autolysosomes. It was confirmed by LysoTracker probe and WB against Beclin 1, APG 5, APG 12 and p53. When autophagy was blocked by 3-MA, not only the protein expression of Beclin 1, but also the antitumor effect of etoposide was suppressed. On the other hand, the addition of zVAD-fmk could induce a few etoposide-induced autophagy. And etoposide-treated CaSki cells were rescued by combination of 3-MA and zVAD-fmk. CONCLUSION: Our results suggest that etoposide not only initiated apoptosis but ultimately caused cell death through autophagy. In this study, we demonstrate novel features for the action of etoposide in HPV-16 (+) CaSki cervical carcinoma cells. Autophagic cell death induction by some anticancer agents underlines the potential utility of its induction as a new cancer treatment modality.

Differential protein expression of etoposide-treated CaSki cervical carcinoma cells / 부인종양

OBJECTIVE: This study was designed to examine the pharmaco-dynamic pattern of proteomic expression in cervical carcinoma cells (CaSki cell line; HPV-16 positive) after in vitro treatment by the etoposide. METHODS: We analyzed proteomic profiling in cervical carcinoma cells after etoposide treatment using two-dimensional gel electrophoresis (2-DE) with MALDI-TOF-MS used for protein identification. Then, we tested the several experimental methods for verification and functional identification, including MTT assay, PI staining, DNA fragmentation assay, FDA, FACS and Western blot analysis. RESULTS: Etoposide inhibited the CaSki cervical cancer cell growth in a dose-dependent manner and the optimal concentration of etoposide is 2micrometer(IC50) in the CaSki cervical cancer cells. The etoposide induced apoptosis, as determined by DNA fragmentation assay, FACS, and Western blot. The etoposide increased the protein expression of Fas (Apo-1/CD95), p53, pRb and caspase-3, but decreased the level of Bcl-2 and caspase-3 precursor and subsequently triggered the mitochondrial apoptotic pathway (release of cytochrome c and activation of caspase-9). To this end, we analyzed CaSki cancer cells using 2-DE. Eight proteins (XAP-5, HXC-36, serine/threonine protein phosphatase 2B catalytic subunit, G2/mitotic-specific cyclin B1, T-box transcription factor TBX20, diacylglycerol kinase, amiloride-sensitive amine oxidase, HEF-like protein, ras-related protein Rab-20) were down-regulated and nine proteins (RNA 3'-terminal phosphate cyclase-like protein, late endosomal/lysosomal Mp1 interacting protein, glia maturation factor, replication protein A 14 kDa subunit, mago sashi protein homolog, 14 kDa phosphohistidine phosphatase, protein C14 or f48, cyclin-dependent kinase 4 inhibitior A, retinoic acid-binding protein II) were up-regulated in etoposide-treated CaSki cells when compared with non-treated cells. CONCLUSION: Our results clearly indicate that etoposide induced cell death by apoptosis. These findings may provide insights into the mechanisms underlying the apparent anti-tumoral effects of etoposide.