Chemotherapy is an essential treatment for breast cancer, inducing cancer cell death. However, chemoresistance is a problem that limits the effectiveness of chemotherapy. Many factors influence chemoresistance, including drug inactivation, changes in drug targets, overexpression of ABC transporters, epithelial-to-mesenchymal transitions, apoptotic dysregulation, and cancer stem cells. The effectiveness of chemotherapy can be assessed clinically and pathologically. Clinical response evaluation is based on physical examination or imaging (mammography, ultrasonography, computed tomography scan, or magnetic resonance imaging) and includes tumor size changes after chemotherapy. Pathological response evaluation is a method based on tumor residues in histopathological preparations. We should be suspicious of chemoresistance if there are no significant changes clinically according to the Response Evaluation Criteria in Solid Tumors and World Health Organization criteria or pathological changes according to the Miller and Payne criteria, especially after 2–3 cycles of chemotherapy treatments. Chemoresistance is mostly detected after the administration of chemotherapy drugs. No reliable parameters or biomarkers can predict chemotherapy responses appropriately and effectively. Well-known parameters such as cancer type, grade, subtype, estrogen receptor, progesterone receptor, human epidermal growth factor receptor 2, Ki-67, and MDR-1/P-gP have been used for selecting chemotherapy regimens. Some new methods for predicting chemoresistance include chemosensitivity and chemoresistance assays, multigene expressions, and positron emission tomography assays. The latest approaches are based on evaluation of molecular processes and the metabolic activity of cancer cells. Some methods for preventing chemoresistance include using the right regimen, using some combination of chemotherapy methods, conducting adequate monitoring, and using drugs that could prevent the emergence of multidrug resistance.

Congenital talipes equinovarus (CTEV) is a congenital disability characterized by leg deformities in the cavus, adducts, varus, and equinus. The etiology of CTEV is poorly understood, despite its incidence ranging from 0.76 to 3.49 cases per 1000 live births in Indonesia. CTEV involves the fixation of the foot in the adducts, varus, and equinus with concurrent soft tissue anomalies. Despite advances in treatment, disability often persists. Theoretical models have been proposed for neurological, vascular, connective tissue, bone, and muscular causes; however, the currently available data suggests that mild cases are associated with intrauterine position. CTEV's etiology appears to involve a hereditary component, as its prevalence varies by ethnic group. Genetic factors have been identified in 24–50% of cases, depending on the community studied. Based on a complex segregation analysis, the most plausible inheritance pattern is a single large-effect gene interacting with a polygenic background.

Introduction: Thermal burns release reactive oxygen species, which cause profound systemic and local changes. Stromal vascular fraction cells (SVFs) combined with platelet-rich plasma accelerate burn wound healing. This study investigated the effect of a combination of locally injected SVFs and PRP on malondialdehyde (MDA) and nitric oxide (NO) serum and tissue levels in a deep dermal burn model in Wistar rats. Methods: Thirty-six adult Wistar rats weighing between 150 and 250 grams were used in this study to establish a deep dermal degree burn wound model. They were randomly divided into 4 groups: locally injected the combination SVFs and PRP, the Vaseline group, the placebo group, and healthy Wistar rats (the normal control group). MDA and NO levels in blood serum and burn wound tissue were measured at 8, 24, and 48 hours. Data were analyzed with one-way ANOVA followed by multiple comparisons tests and regression tests. Results: Local injection of SVFs and PRP in combination affected blood MDA, tissue MDA, blood NO and tissue NO levels, with reductions of 0.257μmol/L, 0.427 μmol/L, 21.78nmol/mg, and 23.777nmol/mg, respectively. Injection of SVFs and PRP in combination reduced tissue MDA levels by 1.282 times, NO blood levels by 2.305, and NO tissue levels by 2.377 times compared to Vaseline application. Conclusion: The combination of SVFs and PRP undeniably reduced the MDA and NO levels in blood and tissue compared to those in the Vaseline and placebo groups. The injection of these two preparations in combination inhibited the local and systemic stress oxidative response, as illustrated by the decreased MDA and NO levels in blood serum and tissue.

The healing process of burns includes coagulation, inflammation, and remodeling. Vascular endothelial growth factor (VEGF) is involved throughout this healing process. Stem cells from the platelet-rich plasma (PRP) with stromal vascular fraction (SVF) can increase concentrations of growth factors, including VEGF. This is expected to accelerate burn healing. The aim of this study was to determine the effect of a combination of PRP and SVF on VEGF levels in a rats model of deep dermal burn wound healing. This is an experimental research study in rats using a post-test control group design with 4 groups: A) control, B) Vaseline, C) topical PRP and SVF, and D) PRP and SVF injection. Burn wounds were induced according to the modified Guo method. In a rats model of deep dermal wound healing, topical Vaseline significantly increased serum VEGF compared to control. Topical application and injection of stem cells also significantly increased serum VEGF compared to control and Vaseline. The VEGF concentration was significantly higher following injection of PRP and SVF, suggesting that the injection route is more effective at increasing VEGF levels compared to the topical application of stem cells. The combination of PRP and SVF, either by injection or topical application, can increase VEGF levels during the healing process from deep dermal burns.

The damaging effects of thermal burns need to be managed holistically in order to create a suitable environment for wound healing. The purpose of our study was to investigate the effects of hyperbaric oxygen therapy (HBOT) on the healing of thermal burns and its relationship with intercellular adhesion molecule 1 (ICAM-1). Twenty patients with thermal burns were randomly divided into two groups: the group to receive HBOT and the control group. Levels of the ICAM-1 mRNA gene and ICAM-1 serum along with the degree of wound epithelialization were examined before and after treatment. Laboratory and physical findings between the groups were compared. In the HBOT group compared with the control group, thermal wound complications were significantly reduced (p = .006), while length of stay in hospital was substantially reduced (p = .001). ICAM-1 serum levels strongly correlated with ICAM-1 mRNA gene expression (R2 = 0.909, p < .001). The expression of the ICAM-1 mRNA gene (12.32 ± 1.31 vs. 10.79 ± 1.38) and ICAM-1 serum level (231.46 ± 37.20 vs. 158.23 ± 68.30) in patients with at least a 50% burn area exceeded those of patients with a smaller burn area. HBOT significantly decreased (p < .05) the expression of the ICAM-1 mRNA gene and ICAM-1 serum level (p = .004). The number of HBOT sessions strongly correlated with ICAM-1 serum level (p = .043) but poorly correlated with ICAM-1 mRNA gene expression (p = .22). The expression of the gene, however, strongly correlated with ICAM-1 serum level (r = −0.988, p < .001). HBOT can reduce thermal wound complications, length of stay in hospitals due to thermal burns, ICAM-1 mRNA gene expression, and ICAM-1 serum level.