AIM OF THE STUDY: To investigate the potential of F3 from S. crispus to prevent metastasis in breast cancer.
MATERIALS AND METHODS: The antimetastatic effects of F3 were first investigated on murine 4T1 and human MDA-MB-231 breast cancer cell (BCC) lines using cell proliferation, wound healing and invasion assays. A 4T1-induced mouse mammary carcinoma model was then used to determine the expression of metastasis tumor markers, epithelial (E)-cadherin, matrix metalloproteinase (MMP)-9, mucin (MUC)-1, nonepithelial (N)-cadherin, Twist, vascular endothelial growth factor (VEGF) and vimentin, using immunohistochemistry, following oral treatment with F3 for 30 days.
RESULTS: Significant growth arrest was observed with F3 IC50 values of 84.27 µg/ml (24 h) and 74.41 µg/ml (48 h) for MDA-MB-231, and 87.35 µg/ml (24 h) and 78.75 µg/ml (48 h) for 4T1 cells. F3 significantly inhibited migration of both BCC lines at 50 μg/ml for 24 h (p = 0.018 and p = 0.015, respectively). Similarly, significant inhibition of invasion was demonstrated in 4T1 (75 µg/ml, p = 0.016) and MDA-MB-231 (50 µg/ml, p = 0.040) cells compared to the untreated cultures. F3 treatment resulted in reduced tumor growth compared to untreated mice (p
STUDY DESIGN: Clinical audit report.
PLACE AND DURATION OF STUDY: Hospital Sultanah Aminah Johor Bahru, Malaysia, from March 2016 to May 2017.
METHODOLOGY: Data were collected retrospectively from all 127 patients who underwent CABG with saphenous vein grafts, either with CVH technique (n=68), or MIVH technique (n=59) performed with Vasoview system. The rate of wound dehiscence was evaluated. Patients with severe wound dehiscence that required readmission and surgical intervention were identified for further evaluation.
RESULTS: There was total 26.8% of wound dehiscence in our study, which was not appreciably different between two groups (p=0.092). Patient with severe wound breakdown that required surgical intervention was significantly less in MIVH group (1/59, 1.7%) compared to CVH group (8/68, 11.8%, p=0.037). There was no significant difference in readmission rate between MIVH and CVH group (p=0.574).
CONCLUSION: There is significant reduction in severity of wound dehiscence post-saphenous vein harvesting among CABG patients with MIVH technique. However, there is no statistical difference in wound dehiscence and readmission rate between MIVH and CVH technique.
METHODS: Wounds were inflicted in type-1 diabetic-streptozotocin (STZ) induced male Sprague Dawley rats. Subsequently, relevant groups were topically treated with the indicated concentrations (12.5, 25 and 50 μM) of VCN-2 hydrocolloid film over the study duration (14 days). The control group was treated with vehicle dressing (blank or allantoin). Wounded tissues and blood serum were collected on 0, 7 and 14 days prior to sacrifice. Appropriate wound assessments such as histological tests, nitric oxide assays, enzyme-linked immunosorbent assays (ELISA) and immunoblotting assays were conducted to confirm wound healing efficacy in the in vivo model. One-way Analysis of Variance (ANOVA) was used for statistical analysis.
RESULTS: Results showed that hydrocolloid film was recapitulated with VCN-2 enhanced diabetic wound healing in a dose-dependent manner. VCN-2 reduced pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α), mediators (iNOS and COX-2), and nitric oxide (NO) via the NF-κB pathway. Data suggests that the VCN-2 film facilitated healing in hyperglycemic conditions by releasing growth factors such as (VEGF and TGF-β) to enhance cell proliferation, migration, and wound contraction via the VEGF and TGF-β mechanism pathways.
CONCLUSIONS: This study's findings suggest that VCN-2 may possess wound healing potential since topical treatment with VCN-2 hydrocolloid films effectively enhanced wound healing in hyperglycemic conditions.
METHOD:: The retrospective study was performed in a referral wound care clinic in Hospital Kuala Lumpur. Data was collected from January 2014 to October 2016 on DFU patients who attended this clinic.
RESULTS:: Of the 340 patients (216 male and 124 female) DFU patients who attended the clinic (mean age: 58.1±10.8 years old), 41.5% presented with infection with a mean cross-sectional ulcer area of 21.5±33.2cm2. Binary logistic regression analysis revealed that patients of Chinese ethnicity (OR: 3.39; 95%CI 1.49 to 7.70), with fasting blood glucose ≥7mmol/l (OR: 3.41; 95%CI 1.57 to 7.39), ulcer size ≥10cm2 (OR: 2.90; 95%CI 1.45 to 5.82) and blood pressure ≥140/90mmHg (OR: 2.52; 95%CI 1.54 to 4.14) were more likely to develop DFI. The median healing time for patients with DFUs was three months. There were six variables identified as significantly associated with prolonged healing time of DFU, namely presence of infection (p<0.001), poor glycaemic control with fasting blood glucose ≥7mmol/l (p<0.001), high blood pressure ≥140/90mmHg (p<0.001), large DFU size ≥2cm2 (p<0.001), history of amputation (p<0.005) and plantar location of the DFU (p<0.05).
CONCLUSION:: Large DFU size, poor glycaemic and blood pressure control are common risk factors for both DFU and DFI. Unexpected high prevalence and ethnicity risk factor for DFI urge more comprehensive primary and secondary preventative strategies to reduce its incidence.
Objective: This study investigated the in vitro and in vivo anti-tumour effects of coconut water vinegar on 4T1 breast cancer cells.
Methods: The 4T1 cells were treated with freeze-dried coconut water vinegar and subjected to MTT cell viability, BrdU, annexin V/PI apoptosis, cell cycle and wound healing assays for the in vitro analysis. For the in vivo chemopreventive evaluation, mice challenged with 4T1 cells were treated with 0.08or 2.00 mL/kg body weight of fresh coconut water vinegar for 28 days. Tumour weight, apoptosis of tumour cells, metastasis and immunity of untreated mice and coconut water vinegar-treated 4T1 challenged mice were compared.
Results: Freeze-dried coconut water vinegar reduced the cell viability, induced apoptosis and delayed the wound healing effect of 4T1 cells in vitro. In vivo, coconut water vinegar delayed 4T1 breast cancer progression in mice by inducing apoptosis and delaying the metastasis. Furthermore, coconut water vinegar also promoted immune cell cytotoxicity and production of anticancer cytokines. The results indicate that coconut water vinegar delays breast cancer progression by inducing apoptosis in breast cancer cells, suppressing metastasis and activating anti-tumour immunity.
Conclusion: Coconut water vinegar is a potential health food ingredient with a chemopreventive effect.
Method: In this study, the potential targets of miR-145 were identified bio-informatically using different target prediction tools. The identified target genes were validated in vitro by dual luciferase assay. Wound healing and soft agar colony assay assessed cell proliferation and migration. miR-145 expression level was measured quantitatively by RT-PCR at different stages of breast tumor. Western blot was used to verify the role of miR-145 in EMT transition using key marker proteins.
Result: Wound healing and soft agar colony assays, using miR-145 over-expressing stably transfected MCF7 cells, unraveled its role as a pro-proliferation candidate in cancerous cells. The association between miR-145 over-expression and differential methylation patterns in representative target genes (DR5, BCL2, TP53, RNF8, TIP60, CHK2, and DCR2) supported the inference drawn. These in vitro observations were validated in a representative set of nodal positive tumors of stage 3 and 4 depicting higher miR-145 expression as compared to early stages. Further, the role of miR-145 in epithelial-mesenchymal (EMT) transition found support through the observation of two key markers, Vimentin and ALDL, where a positive correlation with Vimentin protein and a negative correlation with ALDL mRNA expression were observed.
Conclusion: Our results demonstrate miR-145 as a pro-cancerous candidate, evident from the phenotypes of aggressive cellular proliferation, epithelial to mesenchymal transition, hypermethylation of CpG sites in DDR and apoptotic genes and upregulation of miR-145 in later stages of tumor tissues.