Background: Noncontact Electro Capacitive Cancer Therapy (ECCT) is a novel treatment modality in cancer. Chemokine (C-C motif) ligand 2 (CCL2) has a major role in the outgrowth of metastatic breast cancer. Interleukin 18 (IL18) plays a role in macrophage alteration, which leads to excessive angiogenesis. This study aims to elaborate on the association of CCL2, IL18, IL23α, and TNF-α (tumor necrosis factor-alpha) expression with the anti-proliferative effect of ECCT in rat breast tumor tissue.   Methods: Low intensity (18 Vpp) and intermediate frequency (150 kHz) alternating current-electric field (AC-EF) between two capacitive electrodes were exposed as external EF to a rat cage. Twenty-four rats were divided into four groups of six replicates. Breast tumor tissues were collected from 7, 12-dimethylbenz[a]anthracene (DMBA)-induced rats. Two groups were non DMBA-induced rats without ECCT exposure (NINT) and with (NIT). The other two groups were DMBA-induced rats without ECCT exposure (INT) and with (IT). Mammary glands and breast tumor tissues were collected from each group and preserved. Hematoxylin-eosin and immunohistochemistry staining were performed on paraffin sections of tissues using anti-PCNA, anti-ErbB2, anti-Caspase3, and anti-CD68. CCL2, IL18, IL23α, and TNF-α mRNA relative expressions were analyzed using qRT-PCR. Results: ECCT exposure may cause the reduction of PCNA protein expression as well as ErbB2 on breast tumor tissues, but it causes the increase of Caspase3 and macrophage CD68 protein. In rat breast tumor tissues of IT groups, the mRNA expression of CCL2 and IL18 are significantly down-regulated, in contrast with the up-regulated expression of these cytokines in tumor tissues of the INT group. IL23α and TNF- α expression remained similar in both groups. Conclusion: CCL2 and IL18 expressions have an association with the inhibition of breast tumor cell proliferation affected by ECCT exposure

The G71R mutation is present, but very rare, in Javanese-Indonesians and Malay-Malaysians. Thus, G71R mutation may not contribute to the high incidence of the neonatal jaundice in South-east Asian populations. DHPLC analysis is a very useful method for detecting the G71R mutation.

This study were to evaluate the properties of kefir prepared with a combination of goat milk and black rice extract and its influence on the improvement of β-cells in streptozotocin-nicotinamide (STZ-NA)-induced diabetic rats. Kefir was divided into four groups using the following materials: goat milk (GM), goat milk+inulin (GM+IN), goat milk+black rice extract (1:1)(GM+BRE), and goat milk+black rice extract+ inulin (GM+BRE+IN). After fermentation, all kefir were stored at 4°C for 1 and 7 d, and then were analyzed for microbial, chemical properties and antioxidant activity. Furthermore, three kinds doses of kefir combination from goat milk and black rice extract (GM+BRE) were administered to rats. Thirty male rats 8-12 weeks old were divided into 6 groups: 1) negative control (normal rats); 2) positive control (untreated diabetic rats); 3) diabetic rats fed kefir (1.0 ml); 4) diabetic rats fed kefir (2.0 ml); 5) diabetic rats fed kefir (4.0 ml), and 6) diabetic rats received glibenclamide. After 28 d experiment, the rats were sacrificed for sampling pancreatic tissues. Subtitution of goat milk with black rice extract in kefir fermentation could decrease their pH and increase in radical-scavenging activity. Inulin addition able to increase (p<0.05) in radical-scavenging activity of kefir. Alcohol and total phenolic contents of kefir increased (p<0.05) after 7 d of storage, while the pH decreased. To improve insulin-producing pancreatic β-cells in diabetic rats, it was required at least 2.0 ml dose of kefir combination from goat milk and black rice extract to achieve similar effect to glibenclamide as antidiabetic agent.

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Background: Noncontact Electro Capacitive Cancer Therapy (ECCT) is a novel treatment modality in cancer. Chemokine (C-C motif) ligand 2 (CCL2) has a major role in the outgrowth of metastatic breast cancer. Interleukin 18 (IL18) plays a role in macrophage alteration, which leads to excessive angiogenesis. This study aims to elaborate on the association of CCL2, IL18, IL23α, and TNF-α (tumor necrosis factor-alpha) expression with the anti-proliferative effect of ECCT in rat breast tumor tissue.   Methods: Low intensity (18 Vpp) and intermediate frequency (150 kHz) alternating current-electric field (AC-EF) between two capacitive electrodes were exposed as external EF to a rat cage. Twenty-four rats were divided into four groups of six replicates. Breast tumor tissues were collected from 7, 12-dimethylbenz[a]anthracene (DMBA)-induced rats. Two groups were none DMBA-induced rats without ECCT exposure (NINT) and with (NIT). The other two groups were DMBA-induced rats without ECCT exposure (INT) and with (IT). Mammary glands and breast tumor tissues were collected from each group and preserved. Hematoxylin-eosin and immunohistochemistry staining were performed on paraffin sections of tissues using anti-PCNA, anti-ErbB2, anti-Caspase3, and anti-CD68. CCL2, IL18, IL23α, and TNF-α mRNA relative expressions were analyzed using qRT-PCR. Results: ECCT exposure may cause the reduction of PCNA protein expression as well as ErbB2 on breast tumor tissues, but it causes the increase of Caspase3 and macrophage CD68 protein. In rat breast tumor tissues of IT groups, the mRNA expression of CCL2 and IL18 are significantly down-regulated, in contrast with the up-regulated expression of these cytokines in tumor tissues of the INT group. IL23α and TNF- α expression remained similar in both groups. Conclusion: CCL2 and IL18 expressions have an association with the inhibition of breast tumor cell proliferation affected by ECCT exposure

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Background and Aims: Hyperglycemia increases inflammation in type 2 diabetes mellitus (T2DM).

Background and Aims: Diabetes mellitus is a metabolic disorder characterized by hyperglycemia due to a defect of insulin secretion, insulin action, or both. There are increasing evidence that active compounds of medicinal plants may be used to treat diabetes. The aim of this study is to investigate the effect of a 7-hydroxy-2-(4-hydroxy-3methoxy-phenyl)-chroman-4-one flavonoid compound of the Swietenia macrophylla King seed on homeostatic model assessment of insulin resistance (HOMA-IR), phosphoenolpyruvate carboxykinase (PEPCK) and retinol binding protein-4 (RBP4) gene expression in diabetic rats. Materials and Method: Thirty Wistar rats were used with 5 in each group as follows: 1) normal rats; 2) diabetic rats; 3) diabetic rats with metformin; 4), 5) and 6) diabetic rats with a 7-hydroxy-2-(4-hydroxy-3-methoxy-phenly)-chroman-4one 10, 30 and 90 mg/200 g body weight (BW) respectively. Blood glucose and insulin levels were analyzed before and after treatment. At the end of the study, the liver tissue was removed for quantitative PCR (qPCR) analyses. Results: Blood glucose levels decreased significantly (p<0.05) in diabetic rats with metformin and three different dosages of 7-hydroxy-2-(4-hydroxy-3-methoxy-phenly)-chroman-4-one. Insulin levels increased significantly (p<0.05) in diabetic rats with metformin and diabetic rats with 10 mg/200 g BW of 7-hydroxy-2-(4-hydroxy-3-methoxy-phenly)-chroman-4-one. HOMA-IR value decreased significantly (p<0.05) in diabetic rats with metformin and three different dosages of 7-hydroxy-2-(4-hydroxy-3-methoxy-phenly)-chroman-4-one. There was a significant decrease of PEPCK gene expression in the group with 90 mg/200 g BW of 7hydroxy-2-(4-hydroxy-3-methoxy-phenly)-chroman-4-one. RBP4 gene expression showed a decline, but the difference between groups was not statistically different. Conclusion: These results demonstrated that 7-hydroxy-2-(4-hydroxy-3-methoxy-phenly)-chroman-4one increased insulin and decreased blood glucose level, HOMA-IR value and PEPCK gene expression.