Rong-Yaun Shyu

Strangulated transmesosigmoid hernia: CT diagnosis

We present a rare case of strangulated closed loop small bowel obstruction secondary to a trans-mesosigmoid hernia to emphasize the diagnostic role of computed tomography in patients with no history of previous surgery. The characteristic computed tomographic features showed a cluster of dilated, fluid-filled, U- and C-shaped loops of small bowel entrapped the left posterior and lateral to the sigmoid colon through a defect in the mesosigmoid, which caused anterior and medial displacement of the sigmoid colon.

Growth regulation by all-trans-retinoic acid and retinoic acid receptor messenger ribonucleic acids expression in gastric cancer cells

Retinoic acid has been recognised as a pivotal compound in cell differentiation, proliferation and malignant transformation. We investigated the effects of all-trans-retinoic acid on cell growth and the expression of retinoid nuclear receptor mRNAs in gastric cancer cells in vitro. Cell growth was quantified by measuring total cellular DNA. The growth of two of the five gastric cancer cell lines tested (SC-M1 and TSGH9201) was inhibited by all-trans-retinoic acid at concentrations ranging from 1 x 10(-8) M to 1 x 10(-6) M. Growth inhibition was associated with G0/G1 phase arrest as determined by flow cytometric analysis. Northern blot analysis showed that all five cell lines expressed mRNA for retinoic acid receptors alpha and retinoic x receptor alpha and beta. Retinoic acid receptor beta mRNA was only expressed in TSGH9201 and TMK-1 gastric cancer cell lines. Two RAR gamma mRNA transcripts (3.2 and 3.0 kb) were detected in SC-M1 and TSGH9201 cells. RA-resistant cells had markedly decreased levels of the 3.2 kb RAR gamma transcript. All-trans-retinoic acid had a cytostatic effect on the growth of some gastric cancer cells, which may be associated with the expression of retinoic acid receptors.

All-trans retinoic acid decreases susceptibility of a gastric cancer cell line to lymphokine-activated killer cytotoxicity.

All-trans retinoic acid (RA) was previously shown to regulate the growth of gastric cancer cells derived from the cell line SC-M1. This study was designed to investigate the effect of RA on the sensitivity of SC-M1 cells to lymphokine-activated killer (LAK) activity. RA at the concentration range of 0.001-10 microM was shown to induce SC-M1 cells to exhibit resistance to LAK activity in a dose-dependent manner. A kinetics study indicated that a significantly increased resistance was detected after 2 days of co-culturing SC-M1 cells with RA and reached a maximum after 6 days of culture. Similar results were obtained from two other cancer cell lines: promyelocytic leukaemia HL-60 and hepatic cancer Hep 3B. A binding assay demonstrated that the binding efficacy between target SC-M1 cells and effector LAK cells was not altered by RA. Flow cytometric analyses revealed that RA exhibited no effect on the expression of cell surface molecules, including HLA class I and class II antigens, intercellular adhesion molecule-1 and -2, and lymphocyte function antigen-3. Cell cycle analysis revealed that culture of SC-M1 cells with RA resulted in an increase in G0/G1 phase and a decrease in S phase, accompanied by a decrease in cyclin A and cyclin B1 mRNA as determined by Northern blot analysis. Additionally, RA was shown to enhance the expression of retinoic acid receptor alpha (RAR alpha) in SC-M1 cells, and to have no effect on the expression of RARbeta or RARgamma. Taken together, these results indicate that RA can significantly increase gastric cancer cells SC-M1 to resist LAK cytotoxicity by means of a cytostatic effect through a mechanism relating to cell cycle regulation. The prevailing ideas, such as a decrease in effector to target cell binding, a reduced MHC class I antigen expression or an altered RARbeta expression, are not involved.

Establishment and Characterization of a Human Gastric Carcinoma Cell Line TMC-1

Established cancer cell lines are useful in the study of various cancers. We established a human gastric carcinoma cell line TMC-1 derived from the lymph node of a moderately differentiated adenocarcinoma of the stomach. TMC-1 cells grew in vitro as a mixture of attached and suspension cells, and exhibited spindle or ovoid morphology. They had a population doubling time of 15 h, a plating efficiency of 61%, formed colonies in semisolid agar, secreted the tumor marker CA 19-9, and were tumorigenic in athymic nude mice. The cells expressed E-cadherin and β-catenin. The karyotypic analysis demonstrated hyperdiploid features with a modal chromosome of 53. The cell had the deletion at chromosome 18q and gains at chromosome 2p13–25, 5p15, 5q21–35, 7, 8q24, 9q, 11, 12p, 14q24–32 and 20. Analysis by fluorescence in situ hybridization showed the deletion at 7qtel and duplication at 7q11.2 at the rearranged chromosome 7. Growth of TMC-1 cells was inhibited by 27–32% by interferon-α (2,000 U/ml) and by interferon-γ with an IC50 of 125 U/ml. The cell line is tumorigenic in vivo, and its growth is moderately inhibited by interferon-α and interferon-γ. It can be used to develop new modalities of human gastric cancer treatment.

Visualization of a photopenic lesion secondary to a giant small bowel diverticulum with fecal retention during Meckel's scintigraphy

A 30-year-old man with a second episode of melena had previous workups, including gastroscopy and colonoscopy, that failed to localize a source of bleeding. Tc-99m pertechnetate abdominal scintigraphy showed a giant photopenic lesion in the suprapubic region. An upper gastrointestinal and small bowel series obtained after Meckels scintigraphy showed a huge small bowel divertIculum in the midanterior pelvis. This case shows how a giant small bowel diverticulum with fecal retention can produce images suggestive of a photopenic lesion during Meckels scintigraphy.