• Steel and Composite Structures
• /
• v.48 no.6
• /
• pp.611-623
• /
• 2023

This work considered an optimal control formulation in the sense of Caputo derivatives. The optimality of the fractional optimal control problem. The tumor immune interaction in fractional form provides an excellent tool for the description of memory and hereditary properties of inter and intra cells. So the interaction between effector-cells, tumor cells and are modeled by using the definition of Caputo fractional order derivative that provides the system with long-time memory and gives extra degree of freedom. In addiltion, existence and local stability of fixed points are investigated for discrete model. Moreover, in order to achieve more efficient computational results of fractional-order system, a discretization process is performed to obtain its discrete counterpart. Our technique likewise allows the advancement of results, such as return time to baseline that are unrealistic with current model solvers.

• Asian Oncology Nursing
• /
• v.11 no.2
• /
• pp.108-115
• /
• 2011

Purpose: The purpose of this study was to examine the effects of preoperative pain management education on postoperative pain control in patients with uterine tumor using patient controlled analgesia. Methods: This study used non-equivalent control group non-synchronized design. Data were collected from September, 2008 to March, 2009 at one university hospital in Daegu, Korea. There were 60 participants, 30 in both the experimental and control group. The experimental group was given preoperative pain education using videos, leaflets, and a PCA model. Postoperative pain intensity, frequency of the PCA button being pressed, and doses of additional analgesics were observed through 24 hours postoperative and knowledge of pain and attitude about the use of the pain medicine were measured at 3 days postoperative. Collected data were analyzed using t-test, ${\chi}^2$ test, repeat measured ANOVA, and Bonferroni methods. Results: There were no significant differences in the postoperative pain level between the experimental and control group. Postoperative frequency of the PCA button pressed, doses of additional analgesics, pain knowledge and attitude about the use of the pain medicine of the experimental group were significantly higher than those of the control group. Conclusion: Pain management education is an effective nursing intervention for pain control after surgery.

• Radiation Oncology Journal
• /
• v.12 no.2
• /
• pp.129-141
• /
• 1994

Intracellular ions which have a major role in cellular function have been reported to affect repair of radiation damage. Recently it has been reported that ouabain sensitizes A549 tumor cellls but not CCL-120 normal cells to radiation. Ouabain inhibits the $Na^+-K^+$-pump rapidly thus it increases intracellular Na concentration, Vanadate which is distributed extensively in almost all living organisms is known to be a $Na^+-K^+$-ATPase inhibitors, This study was performed to see any change in radiosensitivity of tumor cell by vanadate and any role of $Na^+-K^+$ATPase in radiosensitization. Experiments have been carried out by pretreatment with vanadate in human cell line(A549, JMG) and mouse cell line(L1210, spleen). For the cell survival MTT assay was performed for A549 and JMC cells and frypan blue dye exclusion test for L120, and spleen cells. Measurements of $Na^+-K^+$-ATPase activity in control, vanadate treated cell, radiation treated cell (9 Gy for A549 and JMG, 2 Gy for L1201, spleen), and combined $10^{-6}M$ vanadate and radiation treated cells were done. The results were summerized as fellows. 1. L1210 cell was most radiosensitive, and spleen cell and JMG cell were intermediate, and A549 cell was least radiosensitive. 2. Mininum or no cytotoxicity was seen with vanadate below concentration of $10^{-6}M$. 3. In A549 cells there was a little change in radiosensitivity with treatment of vanadate. However radiation sensitization was shown in low dose level of radiation i. e. 2- Gy. In JMG cells no change in radiosensitivity was noted. Both L1210 and spleen cell had radiosensitization but change was greater in tumor cell. 4. $Na^+-K^+$-ATPase activity was inhibited significantly in tumor cell by treatment of vanadate. 5. Radiaiton itself inhibited $Na^+-K^+$-ATPase activity of tumor cell with high $Na^+-K^+$-ATPase concention. Increase in radiosensitivity by vanadate was closely associated with orginal $Na^+-K^+$-ATPase contents. From the above results vanadate had little cytotoxicity and it sensitized tumor cells to radiation. Inhibitory effect of vanadate on $Na^+-K^+$-ATPase activity might be one of the contributing factors for radiosensitization to tumor cells which has greater enzyme activity than that of normal cell. It was suggested vanadate could be used as a potential radiosensitizer for tumor cells.

• Radiation Oncology Journal
• /
• v.5 no.1
• /
• pp.23-30
• /
• 1987

Thirty eight patients with stage I and II primary gastrointestinal non-Hodgkin's lymphoma were treated in the Department of Therapeutic Radiology, Seoul National University Hospital between 1979 and 1984. There were 6 systemic disseminations during radiotherapy, and the overall failure rate were $31\%$ in the cases with tumor bulk less than 5cm in diameter before radiotherapy and $75\%$ in the cases with tumor bulk greater than 5cm in diameter (p <0,05). The overall 5 year survival rate were $69.2\%$ in 28 patients who completed radiotherpay and $72\%$ in 24 patients with tumor bulk less than 5cm in diameter (small or no tumor bulk). The 5 year disease free survival rate were $71\%$ in cases with tumor bulk less than 5cm in diameter and $25\%$ in cases with tumor bulk greater than 5cm in diameter (p<0.01). But the intitial stage was not related with treatment result in all cases or subgroups of cases. Thus the cases with small or no tumor bulk were shown to be curable with combined surgery and postoperative radiotherapy, but for the control of the cases with large tumor bulk that had a guarded prognosis combined radiotherapy and chemotherapy should be tried.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.1
• /
• pp.121-126
• /
• 2013

Background: Significance of HPV infection and genic mutation of APC and K-ras in rectal cancer has been investigated but not clarified. The objective of our study was to investigate these parameters in patients with rectal cancer to analyze correlations with biological behaviour, to determine relationships among the three, and also to demonstrate survival prognosis effects. Methods: From December 2007 to September 2008, 75 rectal cancer cases confirmed by histopathology in the Tumor Hospital of Xinjiang Medical University were enrolled. The control group consisted of normal rectal mucous membrane taken simultaneously, a least 10 cm distant from the carcinoma fringe. HPV DNA, the MCR of APC and exon-1 of K-ras were detected by PCR and PCR-SSCP. All results were analyzed in relation to clinical pathological material, using chi-square and correlation analysis via SPSS.13 and Fisher's Exact Probability via STATA. 9.0. All 75 patients were followed up for survival analysis using Kaplan-Meier and Log-rank tests. Results: 55 out of 75 cases demonstrated gene HPV L1 while it was notdetected in normal rectal mucosa tissue. HPV infection was correlated with age and lymphatic metastasis (P<0.05) but not other characteristics, such as ethnicity, tumor size, histological type, tumor type, Duke's stage and infiltration depth. Some 43 cases exhibited APC genic mutation (57.3%) and 34 K-ras genic mutation (45.3%). APC genic mutation was correlated with gender(P<0.05), but not age, histological type, infiltration depth, lymphatic metastasis and Duke's stage. In 55 cases of rectal cancer with HPV infection, there were 31 cases with genic mutation of APC (56.4%) and 24 with genic mutation of K-ras (43.6%). For the 20 cases of rectal cancer with non-HPV infection, the figures were 12 cases (60%) and 10 (50.0%), respectively, with no significant relation. Survival analysis showed no statistical significance for K-ras genic mutation, APC genic mutation or HPV infection (P>0.05). However, the survival time of the patients with HPV infection was a little shorter than in cases without HPV infection. Conclusions: Our results suggest that HPV infection might be an important factor to bring about malignant phenotype of rectal cancer and influence prognosis. Genic mutation of APC and K-ras might be common early molecular events of rectal cancer, but without prognostic effects on medium-term or early stage patients with rectal cancer.

• IMMUNE NETWORK
• /
• v.3 no.3
• /
• pp.211-218
• /
• 2003

Background: Vitamin C is an essential nutrient, taken as a daily supplement by many people. Recently, high-dose vitamin C is considered as a therapeutic regimen in some clinical situations. Until now, few studies have been done with the effects of high-dose vitamin C on the immune response. Methods: In this experiment, the effects of high-dose vitamin C on cell-mediated immune response in immunologically competent mice were evaluated. After intraperitoneal injection of 2.5, 5, or 10 mg/day of vitamin C for 10 days, delayed type hypersensitivity (DTH) was provoked against DNFB in the pinnae as a model for cell-mediated immune response. Severity of DTH reaction was evaluated as the thickness of pinnae, and the vitamin C levels were measured in the serum, liver, kidney, lung, pinnae, and splenocytes. Results: After challenge, the thickness increased at its peak on the $2^{nd}$ day in all groups. On the first day, the pinnae were thicker in the injected groups than in the control. On the contrary, the increment of the pinnae thickness was attenuated and the number of cells infiltrated in the site of DTH decreased proportionately to the amount of vitamin C administered from the second day on. With vitamin C exogenously given, the serum level peaked at 30 min after injection, and returned abruptly to its basal level without accumulation. However, it accumulated in the liver, kidney, and especially in the pinnae inflamed and splenopcytes, proportionately to the amount administered. Conclusion: Based on these results, it is suggested that, in one hand, exogenously administered high-dose vitamin C accumulated in the splenocytes and presumably changed the function of them resulting in the augmented cell-mediated immune response, as was revealed in the first day of DTH reaction. On the other hand, it seems likely that the vitamin C also showed anti-inflammatory effects.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.26 no.5
• /
• pp.687-692
• /
• 2012

Schizandra chinensis extract has been known to possess a variety of efficacy including antitumor. However, it remains unclear how schizandrin, which is a major biological active ingredient of Schizandra chinensis, exerts antitumor effect. This study was designed to investigate the mechanism by which schizandrin inhibits tumor growth and metastasis. In in vivo test using tumor model mice injected with B16BL6 cell line, mice treated with 10 and 100 ${\mu}g/ml$ schizandrin showed a significant inhibition by $73.79{\pm}6.43%$ and $90.46{\pm}1.72%$, respectively, compared with positive tumor controls. Schizandrin did not exert a significant toxicity for the normal cells (HUVECs) and tumor cell lines (A549, B16BL6, Du145, Huh7). Treatment with schizandrin at 10 and 100 ${\mu}g$/head significantly inhibited the tumor-induced angiogenesis by $68.04{\pm}32.21%$ and $103.8{\pm}34.99%$ compared with the positive control group, respectively. Using in vivo lung metastasis model, tumor metastasis assay revealed that 10 and 100 ${\mu}g$/head schizandrin significantly decreased the metastatic lung tumor by $37.51{\pm}8.15%$ and $75.53{\pm}4.38%$ compared with positive controls, respectively. On the other hand, schizandrin did not affect the adherence of B16BL6 cell line to extracellular matrix protein. These results demonstrate that schizandrin exerts inhibitory effect on tumor growth and metastasis by inhibiting angiogenesis. This study thus suggest that schizandrin may be a candidate molecule target for cancer drug development.

• Asian Pacific Journal of Cancer Prevention
• /
• v.16 no.13
• /
• pp.5541-5547
• /
• 2015

Background: The role of surgical resection for patients with single large (${\geq}5cm$) and/or multinodular (${\geq}2$) hepatocellular carcinoma (HCC) is still controversial. This systematic review was performed to evaluate the safety and efficacy of resection for patients with single large and/or multinodular HCC. Materials and Methods: Databases (the PubMed, Web of Science, Embase, and Cochrane databases) were systematically searched to identify relevant studies exploring the safety and efficacy of resection for single large and/or multinodular HCC, published between January 2000 and December 2014. Perioperative morbidity and mortality, overall survival, and disease-free survival of the resection group were calculated. In addition, these outcome variables were also calculated for the control group in the included studies. Results: One randomized controlled trial and 42 nonrandomized studies involving 9,580 patients were eligible for analysis. Eight (1,594 patients) of the 43 studies also reported the outcomes of transarterial chemoembolization (TACE). Although 51.4% of patients featured cirrhosis, 90.7% of them demonstrated Child-Pugh A liver function in the resection group. The median rates of morbidity (24.5%) and mortality (2.5%) after resection were significantly higher than that of TACE (11.0%, P<0.001; 1.9%, P<0.001). However, patients who underwent resection had significantly higher median one-, three-, and five-year overall survival (76.1%, 51.7%, and 37.4%) than those who underwent TACE (68.3%, 31.5%, and 17.5%, all P<0.001). The median 1-, 3-, and 5-year DFS rates after resection were 58.3%, 34.6%, and 24.0%, respectively. Conclusions: Although tumor recurrence after resection for patients with single large and/ or multinodular HCC continues to be a major problem, resection should be considered as a strategy to achieve long-term survival.

• BMB Reports
• /
• v.28 no.6
• /
• pp.556-561
• /
• 1995

The purpose of this study was to establish an in vitro culture method of tumor-specific T cells, and determine the efficacy of the cultured tumor-specific cytotoxic T-lymphocytes (CTL) as an agent of anti-tumor immunotherapy against a murine lymphoma, TIMI.4. Tumor-specific T-lymphocytes derived from C57BL/6 mice (thy-1.2) immune to TIMI.4 were activated by in vitro stimulation with the irradiated TIMI.4 cells, and expanded by restimulation with TIMI.4 in the presence of the concanavalin A-stimulated rat spleen culture supernatant, and splenic antigen-presenting cells. In vitro restimulation enhanced markedly the proportion of $CD8^+$, a predominant surface marker of CTL and the cytotoxic activity in the cultured immune T cell population. The resulting TIMI.4-specific T cells were adoptively transferred into nude mice. The tumor cells residing in the host after 7 days of adoptive transfer to B6.PL (thy-1.1) mice were quantified by use of an antibody directed to the thy-1.2 allele. The TIMI.4 cells in the recipient nude mice were decreased in a dose-dependent manner. Anti-tumor activity of the TIMI.4-specific T cells was also demonstrated by a survival test, where the tumor-bearing nu/nu mice which received the activated T-cells survived about 30% longer than the control mice which received the tumor cells alone. These suggest that adoptive transfer of TIMI.4-specific T cells could be a candidate for effective therapy of the murine lymphoma.

• Journal of Life Science
• /
• v.34 no.6
• /
• pp.418-425
• /
• 2024

Solid tumors are heterogeneous populations of multiple cell types. While the majority of the cells that comprise cancer are unable to divide, cancer stem cells have self-renewal and differentiation properties. Normal stem cell pathways that control self-renewal are overactivated in cancer stem cells, making cancer stem cells important for cancer cell expansion and progression. Dick first proposed the definition of cancer stem cells in acute myeloid leukemia, according to which cancer stem cells can be classified based on the expression of cell surface markers. Cancer stem cells maintain their potential in the tumor microenvironment. Multiple cell types in the tumor microenvironment maintain quiescent cancer stem cells and serve as regulators of cancer growth. Since current cancer treatments target proliferative cells, quiescent state cancer stem cells that are resistant to treatment increase the risk of recurrence or metastasis. Various signals of the tumor microenvironment induce changes to become a tumor-supportive environment by remodeling the vasculature and extracellular matrix. To effectively treat cancer, cancer stem cells and the tumor microenvironment must be targeted. Therefore, it is important to understand how the tumor microenvironment induces reprogramming of the immune response to promote cancer growth, immune resistance, and metastasis. In this review, we discuss the cellular and molecular mechanisms that can enhance immunosuppression in the tumor microenvironment.