METHODS: PubMed, Web of Science, and Google Scholar databases were explored to find related articles. Search terms were amputees, artificial limb, prosthetic suspension, prosthetic liner, vacuum, and prosthesis. The results were refined by vacuum socket or vacuum assisted suspension or sub-atmospheric suspension. Study design, research instrument, sample size, and outcome measures were reviewed. An online questionnaire was also designed and distributed worldwide among professionals and prosthetists (www.ispoint.org, OANDP-L, LinkedIn, personal email).
FINDINGS: 26 articles were published from 2001 to March 2016. The number of participants averaged 7 (SD=4) for transtibial and 6 (SD=6) for transfemoral amputees. Most studies evaluated the short-term effects of vacuum systems by measuring stump volume changes, gait parameters, pistoning, interface pressures, satisfaction, balance, and wound healing. 155 professionals replied to the questionnaire and supported results from the literature. Elevated vacuum systems may have some advantages over the other suspension systems, but may not be appropriate for all people with limb loss.
INTERPRETATION: Elevated vacuum suspension could improve comfort and quality of life for people with limb loss. However, future investigations with larger sample sizes are needed to provide strong statistical conclusions and to evaluate long-term effects of these systems.
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.
DESIGN: A single-center, randomized controlled trial.
METHODS: A total of 132 patients with uncomplicated phacoemulsification were randomly allocated to the intervention or control group. The intervention group received postoperative eye patching for approximately 18 hours, whereas the control group received eye shield. The clear corneal incision architecture was examined postoperatively at 2 hours, 1 day, and 7 days after surgery using optical coherence tomography.
RESULTS: Epithelial gaping was significantly reduced on postoperative day 1 in the intervention group (52.4%) compared with control (74.2%) (P = 0.01). No differences were found for other architectural defects. Descemet membrane detachment was associated with lower intraocular pressure on postoperative day 7 (P = 0.02). Presence of underlying diabetes mellitus did not seem to influence architectural defects.
CONCLUSIONS: Postoperative eye patching facilitated epithelial healing and reduced the occurrence of epithelial gaping on postoperative day 1. It may play a role in protecting and improving corneal wounds during the critical immediate postoperative period.
Methods: Autologous whole blood collected 72 h before surgery was processed to prepare platelet concentrates and cryoprecipitate. In a closed system, calcium was added to the cryoprecipitate to release autologous thrombin and generate a firm fibrin clot. The fibrin clot, platelets and calcium were then placed in a conical flask in which a PRF glue formed. The protocol was validated through determination of pre- and post-platelet counts and fibrinogen amounts in the product.
Results: Platelets were recovered with 68% efficiency during the preparation. Essentially no platelets or fibrinogen were found in the supernatant of the PRF glue, suggesting that nearly all had been incorporated in a PRF glue having a relatively large (8 cm × 10 cm) size.
Conclusion: The protocol described here is a cost-effective, simple and closed system that can be used to produce large-size PRF glue to promote repair of major surgical defects.
METHODS: This double blinded randomized controlled trial was conducted in University Malaya Medical Centre between October 2019 and March 2022. Patients undergoing emergency laparotomy requiring incisions less than 35 cm were included. Statistical analysis was performed using χ2 test for categorical variables, independent T-test or Mann-Whitney U were used for parametric or non-parametric data respectively besides logistic regression. P values of wound care experience, and was associated with trends towards fewer wound related complications. Cost effectiveness needs to be explored in order to further validate its use in the emergency setting, especially for patients with additional risk for SSI. Trial registration National Medical Research Registry (NMRR): NMRR-20-1975-55222.
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
METHODS: Gene expression of IL-6 and IL-6Rα in PSC and PDAC cells was measured with qRT-PCR. The role of PSC-secreted IL-6, JAK/Stat3 signaling, and Nrf2 mediation on EMT-related genes expression was also examined with qRT-PCR. EMT phenotypes were assessed with morphological change, wound healing, migration, and invasion.
RESULTS: PSC expressed higher mRNA levels of IL-6 but lower IL-6Rα compared to PDAC cells. Neutralizing IL-6 in PSC secretion reduced mesenchymal-like morphology, migration and invasion capacity, and mesenchymal-like gene expression of N-cadherin, vimentin, fibronectin, collagen I, Sip1, Snail, Slug, and Twist2. Inhibition of JAK/Stat3 signaling induced by IL-6 repressed EMT and Nrf2 gene expression. Induction of Nrf2 activity by tert-butylhydroquinone (tBHQ) increased both EMT phenotypes and gene expression (N-cadherin, fibronectin, Twist2, Snail, and Slug) repressed by IL-6 neutralizing antibody. Simultaneous inhibition of Nrf2 expression with siRNA and Stat3 signaling further repressed EMT gene expression, indicating that Stat3/Nrf2 pathway mediates EMT induced by IL-6.
CONCLUSIONS: IL-6 from PSC promotes EMT in PDAC cells via Stat3/Nrf2 pathway.
GENERAL SIGNIFICANCE: Targeting Stat3/Nrf2 pathway activated by PSC-secreted IL-6 may provide a novel therapeutic option to improve the prognosis of PDAC.