No abstract available.
Immunoglobulin Light Chains* ; Lymphoma, B-Cell, Marginal Zone*

Extranodal marginal zone B-cell lymphoma of mucosa associated lymphoid tissue (MALT lymphoma) is a low-grade B-cell lymphoma that presents with an indolent clinicopathologic nature. Although this tumor can occur in various sites, including the gastrointestinal, skin, salivary gland and ocular adnexa, radiation therapy shows high local control in that disease. We report a case of recurrent MALT lymphoma presenting a huge cheek mass after radiotherapy on ocular adnexal lymphomas. An 65-year-old man had a history of treatments on MALT lymphomas of ocular adnexa came again with a huge cheek mass, not recurred and not originated from salivary gland, skin, other related mucosa tissues. He got excisional biopsy and was confirmed immunohistochemically as MALT lymphoma. After diagnosis, he was sent urgently to a radiotherapist for further treatment. He responded well to added radiotherapy with 36 Gy dose and has remained well at 6 months after his initial presentation.
Aged ; Biopsy ; Cheek ; Head and Neck Neoplasms ; Humans ; Lymphoid Tissue ; Lymphoma ; Lymphoma, B-Cell ; Lymphoma, B-Cell, Marginal Zone ; Mucous Membrane ; Porphyrins ; Salivary Glands ; Skin

BACKGROUND: Two tumor suppressor genes, p53 and p16, which have different roles in controlling the cell cycle and inducing apoptosis, are frequently inactivated during carcinogenesis including lung cancer. Single tumor suppressor gene therapies using tither with p53 or p16 have been studied extensively. However, there is a paucity of reports regarding a combined gene therapy using these two genes. METHODS: The combined effect of p53 and p16 gene transfer by the adenoviral vector on the growth of lung cancer cell lines and its interactive mechanism was investigated. RESULTS: An isobologram showed that the co-transduction of p53 and p16 exhibited a synergistic growth inhibitory effect on NCI H358 and an additive effect on NCI H23. Cell cycle analysis demonstrated the induction of a synergistic G1/S arrest by a combined p53 and p16 transfer. This synergistic interaction was again confirmed in a soft agar clonogenic assay. CONCLUSION: These observations suggest the potential of a p53 and p16 combination gene therapy as another potent strategy in cancer gene therapy.
Adenoviridae ; Agar ; Apoptosis ; Carcinogenesis ; Cell Cycle ; Cell Line* ; Genes, Neoplasm ; Genes, p16 ; Genes, Tumor Suppressor ; Genetic Therapy ; Lung Neoplasms* ; Lung*

BACKGROUND: One of the important mechanisms responsible for a tumor escaping the immune response is an absence of the tumor associated antigen (TAA) on the cancer cell surface. To overcome this, combination gene therapy using a herpes simplex thymidine kinase (HSTK) gene, prototype of drug sensitizing gene, was conducted to enhance TAA release by cell destruction, as well as the cytokine genes for immune cell attraction. METHODS: We investigated whether or not transduction with the adenovirus-HSTK (Ad-HSTK) enhanced the sensitivity of Lewis lung carcinoma (LLC) to ganciclovir (GCV) and induced a bystander effect. A Tumor vaccine trial was performed using LLC with ad-HSTK ±ad-GM-CSF±ad-IL-2 to determine if they exhibit some antitumor effect on established lung cancer xenografts. RESULTS: LLC with ad-HSTK revealed a much higher sensitivity to ganciclovir (GCV). LLC transduced with ad-HSTK and/or ad-IL-2, ad-GM-CSF showed a lower in vivo tumorigenicity. In the treatment experiment, vaccination with LLC transduced with ad-HSTK, ad-IL-2, or ad-GM-CSF alone modestly suppressed the growth of an established tumor. Combined transduction with HSTK and GM-CSF induced stronger growth suppression of a established lung cancer, while HSTK and IL-2 combination transduction did not have any antitumor effect on individual transduction. Vaccination with LLC-HSTK-GM-CSF increased the infiltration of dendritic cells in the spleen. CONCLUSION: It was concluded that a tumor vaccine transduced with HSTK and GM-CSF induces strong antitumor immunity by activating the dendritic cells.
Adenoviridae ; Animals ; Bystander Effect ; Carcinoma, Lewis Lung ; Cytokines* ; Dendritic Cells ; Ganciclovir ; Genetic Therapy* ; Granulocyte-Macrophage Colony-Stimulating Factor ; Herpes Simplex* ; Heterografts ; Interleukin-2 ; Lung Neoplasms* ; Lung* ; Phosphotransferases* ; Simplexvirus* ; Spleen ; Thymidine Kinase ; United Nations ; Vaccination

This retracts the below mentioned article upon the authors' request.

BACKGROUND: Propofol can produce a dose-dependent reduction in blood pressure by providing titratable sedation and rapid recovery. It has been reported that a combination of midazolam and propofol resulted in the significant reduction in the total dose of propofol needed. It was hypothesized that the addition of low-dose midazolam to propofol may provide sufficient sedation without compromising the hemodynamic stability. METHODS: A total of 40 consecutive patients were randomly assigned to one of two groups (n = 20 each). Group M-P received a bolus of 0.02 mg/kg of midazolam, followed by a propofol infusion with a fixed target concentration of 1.0microgram/ml. Group P received only a propofol infusion with an initial target plasma concentration of 2.5microgram/ml. Subsequent titration of the infusion rates in Group P or the additional midazolam boluses in Group M-P were made in order to maintain a predetermined sedation level. RESULTS: In Group P, a mean dose of 5.4 +/- 0.7 mg/kg/h propofol was used compared with 2.7 +/- 0.5 mg/kg/h in Group M-P (P<0.0001, plus additional 2.96 +/- 1.8 mg of midazolam). Ephedrine was administered to 15 patients in Group M-P and 17 patients in Group P. Recovery was significantly fast (Group P, 6.8 +/- 2.9 min vs. Group M-P, 9.8 +/- 4.4 min, P<0.05). CONCLUSIONS: Sedation with propofol plus midazolam requires a lower total dose of propofol compared with propofol alone but has no superior hemodynamic stability. A further study using younger patients and combinations of different doses of each drug will be needed.
Anesthesia, Spinal* ; Blood Pressure ; Ephedrine ; Hemodynamics ; Humans ; Hypotension ; Midazolam ; Plasma ; Propofol* ; Prospective Studies*

Mainly due to the slanted focus on the mechanism and regulation of neuronal aging, research on astrocyte aging and its modulation during brain aging is scarce. In this study, we established aged astrocyte culture model by long-term culturing. Cellular senescence was confirmed through SA-β-gal staining as well as through the examination of morphological, molecular, and functional markers. RNA sequencing and functional analysis of astrocytes were performed to further investigate the detailed characteristics of the aged astrocyte model. Along with aged phenotypes, decreased astrocytic proliferation, migration, mitochondrial energetic function and support for neuronal survival and differentiation has been observed in aged astrocytes. In addition, increased expression of cytokines and chemokine-related factors including plasminogen activator inhibitor -1 (PAI-1) was observed in aged astrocytes. Using the RNA sequencing results, we searched potential drugs that can normalize the dysregulated gene expression pattern observed in long-term cultured aged astrocytes. Among several candidates, minoxidil, a pyrimidine-derived anti-hypertensive and anti-pattern hair loss drug, normalized the increased number of SA-β-gal positive cells and nuclear size in aged astrocytes. In addition, minoxidil restored up-regulated activity of PAI-1 and increased mitochondrial superoxide production in aged astrocytes.We concluded that long term culture of astrocytes can be used as a reliable model for the study of astrocyte senescence and minoxidil can be a plausible candidate for the regulation of brain aging.

BACKGROUND: Some chemotherapeutic drugs induce NF-κB activation by degrading the IκBα protein in cancer cells which contributes to anticancer drug resistance. We hypothesized that inhibiting IκBα degradation would block NF-κB activation and result in increased tumor cell mortality in response to chemotherapy. METHODS: The "superrepressor" form of the NF-κB inhibitor was transferred by an adenoviral vector (Ad-IκBα-SR) to the human lung cancer cell lines (NCI H157 and NCI H460). With a MTT assay, the level of sensitization to cisplatin and paclitaxel were measured. To confirm the mechanism, an EMSA and Annexin V assay were performed. RESULTS: EMSA showed that IκBα-SR effectively blocked the NF-κB activation induced by cisplatin. Transduction with Ad-IκBα-SR resulted in an increased sensitivity of the lung cancer cell lines to cisplatin and paclitaxel by a factor of 2~3 in terms of IC50. Annexin-V analysis suggests that this increment in chemosensitivity to cisplatin probably occurs through the induction of apoptosis. CONCLUSION: The blockade of chemotherapeutics induced NF-κB activation by inducing Ad-IκBα-SR, increased apoptosis and increasing the chemosensitivity of the lung cancer cell lines tested, subsequently. Gene transfer of IκBα-SR appears to be a new therapeutic strategy of chemosensitization in lung cancer.
Adenoviridae ; Annexin A5 ; Apoptosis ; Cell Line* ; Cisplatin ; Drug Resistance ; Drug Therapy ; Humans* ; Inhibitory Concentration 50 ; Lung Neoplasms* ; Lung* ; Mortality ; Paclitaxel*

BACKGROUND/AIMS: Reflux esophagitis is a recurring condition for which many patients require maintenance therapy. This comparative, randomized multicenter study was designed to evaluate the effect of long-term maintenance treatment comparing proton pump inhibitor, rabeprazole and H2 receptor antagonist, ranitidine. METHODS: Eighty four patients with healed reflux esophagitis confirmed by endoscopy were randomly allocated to receive maintenance treatment with either rabeprazole 10 mg once daily or ranitidine 300 mg once daily for 32 weeks. Patients were seen every 8 weeks or at symptomatic relapse. RESULTS: Of 84 initially treated patients, 73 entered the maintenance study. The percentage of asymptomatic patients after 90-day and 210-day treatment were 97% and 81.5%, for rabeprazole and 74.3% and 62.3%, for ranitidine, respectively. After 32 weeks, the relapse rates of esophagitis were 21.3% in the rabeprazole group and 62.9% in the ranitidine group (RR: 0.405, 95% CI: 0.215-0.766). CONCLUSIONS: Maintenance treatment with rabeprazole (10 mg once daily) is superior to ranitidine (300 mg once daily) in keeping the patients with reflux esophagitis in remission over a 32 week period.
2-Pyridinylmethylsulfinylbenzimidazoles ; Adult ; Anti-Ulcer Agents/*therapeutic use ; Benzimidazoles/*therapeutic use ; Esophagitis, Peptic/*drug therapy ; Female ; Humans ; Male ; Middle Aged ; Omeprazole/*analogs & derivatives/therapeutic use ; Ranitidine/*therapeutic use

PURPOSE: TGF-beta-1 is actually a major growth inhibitor for most cell types. We assumed that the loss of TGF-beta-1 would be occurred during carcinogenesis of the lung. Also, the mutation and expression of p53 have been known to be major moleclar change of non-small cell carcinoma of the lung. So, the relationship between the mutation of p53 and the expression of TGF-beta-1 in the non-small cell carcinomas were evaluated. MATERIALS AND METHODS: In 43 non-small cell carcinoma and normal tissue of the lung, their TGF-beta-1 mRNA were measured by RT-PCR and p53 was studied by SSCP and Western blotting assay. RESULTS: p53 mutation rate in non-small cell carcinomas of the lung (48.4%) was much more frequent than the normal control group (14.3%). The expression rate of TGF-beta-1 in lung carcinomas, especially squamous cell carcinoma (71.4%), was much higher than the normal control group (42.9%). p53 mutation and TGF-beta-1 mRNA in the lung carcinomas were not strongly correlated. CONCLUSION: It suggests that high expression rate of TGF-beta-1 and p53 mutation are associated with carcinogenesis of non-small cell carcinoma of the lung. High expression rate of TGF-beta-1 in the lung carcinomas can be partly explained by the fact that TGF-beta-1 have capacity to control the production of many components of the extracellular matrix and enhance angiogenesis in favor of tumor growth despite of their inhibitory effects of cell growth. However, additional research is required to determine the exact role of TGF-beta-1 in carcinogenesis of the lung.
Blotting, Western ; Carcinogenesis ; Carcinoma, Squamous Cell ; Extracellular Matrix ; Lung* ; Mutation Rate ; Polymorphism, Single-Stranded Conformational ; RNA, Messenger ; Transforming Growth Factor beta1*