Biomedical subjects

M Wang

Publications and source records attributed to M Wang.

1,123 records · Page 63Linked to original sources

PubMedDate not supplied

Interleukin-2 enhances susceptibility of colon cancer cells to FasR mediated apoptosis by up-regulating Fas receptor level and down-regulating FAP-1 expression.

Colon cancer cells are resistant to FasR-mediated apoptosis, which contributes to their evasion from immune attack by CTLs and NK cells. FasR refractoriness of the malignancies was reported to result from loss of Fas receptors and overepression of Fas-associated phosphatase-1 (FAP-1). Therefore, we investigated the effects of recombinant IL-2 on FasR and FAP-1 expression of colon cancer cells, and its influence on the sensitivity of colon cancer cells to FasR-mediated apoptosis. Colon cancer cell lines SW480, HT-29 and CaCo2 were incubated with IL-2 for different periods of time. Sensitivity of the cells to FasR-mediated apoptosis was assessed by measuring their apoptosis after treated with agonistic anti-FasR MAb CH-11. Additionally, Fas receptor levels were examined by immunofluorescence and mRNA expression of FasR and FAP-1 was investigated by RT-PCR: IL-2 incubation increased CH11-induced apoptosis in all colon cancer cell lines in a time-dependent manner. In parallel, IL-2 up-regulated Fas receptor expression on HT29 and CaCo2 cells at both protein and mRNA levels, which were low before treatment, while it served to maintain high expression of FasR on SW480 cells. Additionally, IL-2 down-regulated FAP-1 mRNA expression on SW480 and CaCo2 cells, which was high before treatment. However, low expression of FAP1 on HT-29 cells remained stable after IL-2 treatment. Thus, IL-2 enhances susceptibility of colon cancer cells to FasR-mediated apoptosis by up-regulating Fas receptor levels and by down-regulating FAP-1 expression, which accounts for its therapeutic effects on abolishing immune evasion in colon cancer cells.

Journal Article↗

PubMedDate not supplied

Synovial excrescences and cysts of the spine: clinicopathological features and contributions to spinal stenosis.

Synovial cysts occur throughout the body and are generally benign lesions with limited clinical consequences. Juxtafacet cysts of the spine, in contrast, often press on a nerve root as it exits in the foramen, causing radiculopathy. Synovial tissue that emanates from the facet joint but extends medially, is an additional important cause of spinal stenosis. Over the past 5 years, neurosurgeons at our institution have operated on a large number of patients with back pain, with removal of abnormal synovial tissues. Histological examination of these tissues distinguishes the different types of pathologic processes responsible for producing symptoms. Juxtafacet cysts may be either mucin-filled ganglion cysts devoid of cyst lining or true synovial cysts with watery content and lined by synovial cells. Ganglion cysts arise in degenerated ligament at the facet joint, and occasionally within synovial stroma. Synovial cysts arise within synovium and, unlike synovial cysts in the extremities, have a thick wall containing granulation tissue, numerous histiocytes and giant cells. This hyperplastic, irritated synovium of the spine, which we term "synovial excrescences", is voluminous and this reactive part overshadows the cystic portion of the lesion in most instances. Iron pigment deposition and inflammation are mild to absent, making synovial excrescences different from pigmented villonodular synovitis. Synovial excrescences of the spine are an important cause of spinal stenosis, predominantly in elderly patients. Surgical removal of excrescences protruding into the spinal canal provides prompt and durable relief of symptoms, usually without the need for extensive bony laminectomy or spinal fusion. Several patients in our study had both spinal ganglion cysts and synovial excrescences, suggesting common risk factors for both lesions.

Aged↗

PubMedDate not supplied

Immunofluorescent studies of the anti-microtubule effects of the anti-cancer drug estramustine.

Immunofluorescent studies in human prostatic carcinoma cells (DU 145) and cultured squirrel fish epithelial cells (a non-cancer cell) revealed that estramustine, a conjugate of estradiol and nor-nitrogen mustard, possessed microtubule disassembly properties. Sixty microM estramustine produced disassembly at both the proximal and distal ends of microtubules, producing short pieces of less than 2 microM which were "wavy" and oriented in a random manner. With increased time of drug exposure these short microtubules disappeared, to be accompanied by a gradual disassembly of a small population of longer microtubules (greater than 7-8 microM). In dividing DU 145 cells it was possible to show a different degree of sensitivity of specific microtubule-containing cellular structures. In mitotic figures the asters were most sensitive and disappeared completely following exposure to estramustine. These were followed by the "pole-to-pole" and "chromosomal" fibers. In cytokinesis, the intercellular fibers between daughter cells were comparatively resistant to the drug. Estramustine did not induce disassembly of the vimentin filaments in non-dividing or dividing cells but did cause their collapse around the nucleus or the mitotic apparatus. These data suggest that specific microtubules have differing sensitivity to estramustine.

Cells, Cultured↗

PubMedDate not supplied

Internal fixation of slipped femoral capital epiphyses.

The problems related to internal fixation for the treatment of slipped femoral capital epiphyses were reviewed in 164 cases and by a questionnaire of 59 orthopedic surgeons. Significant problems were reported with all fixation devices. With Trifin nails, the main difficulty was getting them to stay in in place. With threaded pins, there was difficulty removing them. The best fixation was obtained with the cast Vitallium Knowles pin, but it requires additional modification and improvement.

Bone Nails↗

PubMedDate not supplied

Liver tumorigenesis by Helicobacter hepaticus: considerations of mechanism.

A new animal model for the causation of liver tumors via a bacterial infection presented itself fortuitously in the form of a new species, Helicobacter hepaticus. This species of Helicobacter colonizes the hepatic bile canaliculi in susceptible strains of mice, resulting in hepatitis and hepatocellular and hepatocholangiolar adenomas and carcinomas. The mechanism by which this infection leads to cancer is unknown. Tests with Helicobacter hepaticus have revealed thus far that the bacteria do not secrete a mutagen which is capable of detection by the Ames Assay. Measurement of oxidatively damaged bases in the liver DNA of hepaticus infected mice have shown accumulation of 8-oxodeoxyguanosine with disease progression. Other promutagenic DNA lesions, 7-methylguanine and O6-methylguanine, indicative of nitrosation of endogenous amines by nitric oxide, were not detected. Analysis of carcinomas and adenomas taken from H. hepaticus infected A/JCr mice revealed no mutations in ras oncogenes or in exons 5-8 of the p53 gene. These preliminary results indicate that a non-genotoxic tumor promotion mechanism, possibly implemented by reactive oxygen species from the immune response, is more likely than a genotoxic mechanism.

Alkylation↗

PubMedDate not supplied

New flexible growth function and its application to the growth of small mammals.

The function [formula: see text] where a is the upper asympotic weight and b, c, k are constants, is derived as a new flexible growth equation and evaluated using commonly applied growth functions such as Monomelecular, Gompertz, Logistic, Richards, France, Janoschek and Hill. Three sets of observations on growth of small mammal species (Microtus brandti and Ochotona curzoniae) are used to evaluate the fits of these functions. In addition, points of inflexion of these growth equations are also derived in this paper. The new function encompasses the Logistic and Monomolecular equation for different value of parameter b. It provides a flexible growth equation capable of describing smooth sigmoidal and diminishing returns behaviour. The success of the new equation in describing these sets of growth patterns underlines its credentials as a suitable additional growth function.

Aging↗

PubMedDate not supplied

Use of a tissue-specific promoter for targeted expression of the herpes simplex virus thymidine kinase gene in cervical carcinoma cells.

Molecular chemotherapy strategies have been developed for a number of epithelial malignancies based on selective delivery and expression of a toxin-encoding gene into the cancer cells. To date, these strategies have not been explored in the context of carcinoma of the cervix, despite the fact that a variety of factors suggest this as an appropriate disease for this gene therapy approach. One limitation in this respect is that appropriate tissue-specific promoters for selective toxin gene expression have not been defined for cervical carcinoma. In this regard, the secretory leukoprotease inhibitor (SLPI) gene has been shown to be constitutively expressed in many epithelial carcinoma cells including the uterine cervix. Thus, we investigated the utility of the SLPI gene as a tissue-specific promoter for regulatory control of the herpes simplex virus thymidine kinase gene for in vitro treatment of cervical carcinoma cells. For this analysis, a gene construct was derived with the herpes simplex virus thymidine kinase gene under regulatory control of the 5' upstream regions of the SLPI gene. Transient transduction of three human cervical carcinoma cell lines with the SLPI-thymidine kinase (TK) construct was followed by treatment with the prodrug ganciclovir. Crystal violet staining was subsequently used to assess cell viability. In this analysis, it was shown that the SLPI-TK construct directed TK-mediated killing in two of three tested cervical cell lines, with the two cell lines being positive for SLPI. In addition, mixing experiments established that cervical carcinoma cells could exhibit a bystander effect which potentially augments the efficacy of molecular chemotherapy approaches. These findings may allow for the development of efficacious, target-specific, toxin gene therapy strategies for cervical carcinoma in human patients.

Carcinoma↗