A QUICK OVERVIEW OF NANOMEDICINE APPLICATIONS IN BREAST CANCER DETECTION, IMAGING, AND THERAPY

Breast cancer continues to be a global public health dilemma and is currently the most prevalent tumor in the world. Breast cancer awareness, public attention, and progress in the breast imaging have had a positive impact on breast cancer recognition and screening. Breast cancer is a fatal disease in females and the leading cause of death in females. Over the past two decades, studies related to breast cancer have guided amazing advances in our understanding of breast cancer, leading to more competent treatments. Among all the malignant diseases, breast cancer is one of the most common causes of mortality among postmenopausal women, accounting for 23% of all cancer fatalities. This is a global problem today, but it is still diagnosed in its advanced stages due to women's neglect concerning about the self-inspection and clinical examination of the breast. This review presents different types of breast cancer, symptoms, risk factors, epidemiology of breast cancer, stages of breast cancer, diagnostic investigations, and treatment. Chemotherapy, targeted therapies, surgery, radiation therapy, hormone replacement therapy, complementary therapies, gene therapy, and stem-cell therapy are some of the treatments for breast cancer. In this review, various applications of nano-carriers were discussed such as nanopolymers, Nanoshells, nanocrystals, quantum dots, and dendrimers were examined, as well as their potential in early cancer diagnosis and therapy

Solvent contribution to the stability of a physical gel characterized by quasi-elastic neutron scattering

The dynamics of a physical gel, namely the Low Molecular Mass Organic Gelator {\textit Methyl-4,6-O-benzylidene-$\alpha$ -D-mannopyranoside ($\alpha$-manno)} in water and toluene are probed by neutron scattering. Using high gelator concentrations, we were able to determine, on a timescale from a few ps to 1 ns, the number of solvent molecules that are immobilised by the rigid network formed by the gelators. We found that only few toluene molecules per gelator participate to the network which is formed by hydrogen bonding between the gelators' sugar moieties. In water, however, the interactions leading to the gel formations are weaker, involving dipolar, hydrophobic or $\pi-\pi$ interactions and hydrogen bonds are formed between the gelators and the surrounding water. Therefore, around 10 to 14 water molecules per gelator are immobilised by the presence of the network. This study shows that neutron scattering can give valuable information about the behaviour of solvent confined in a molecular gel.Comment: Langmuir (2015

Recovery timeline following resistance training in professional female soccer players

© 2020 Informa UK Limited, trading as Taylor & Francis Group. Objective: Determine the time-course of recovery after a resistance training session (RT) in female soccer players. Methods: Ten Brazilian female professional soccer players undertook testing prior to and at immediately, 24 and 48 h post-RT. RT was a high-speed and low-load session, consisting of three sets of six repetitions of lower body exercises at 50%1RM. Tests included countermovement jump (CMJ) and 20 m sprint, with the best and mean efforts recorded. Delayed onset muscle soreness (DOMS), total quality recovery (TQR) and Brazilian Mood Scale (BRAMS) were collected. Repeated measures ANOVA with effect sizes (ES) assessed the time-course of recovery (α=0.05). Results: Mean and best CMJ performance decreased immediately post-RT (p0.05, ES=−0.15; −0.08) and 48h (p>0.05, ES=0.14; −0.21). No significant differences and trivial-small effects were evident at any time for mean or best 10m (p>0.05, ES=−0.18–0.26) or 20m (p>0.05, ES=−0.08–0.19) performance. DOMS, TQR, fatigue and vigor did not change following RT (p>0.05; ES=-0.51-0.48). Conclusion: Light-load, high-speed RT induces only small, immediate changes in CMJ, without prolonged suppression of recovery parameters. Such training seems feasible for inclusion in competitive micro-cycles at least 24h prior to the next match

Identification of the site of oxidase substrate binding in Scytalidium thermophilum catalase.

The catalase from Scytalidium thermophilum is a homotetramer containing a heme d in each active site. Although the enzyme has a classical monofunctional catalase fold, it also possesses oxidase activity towards a number of small organics, including catechol and phenol. In order to further investigate this, the crystal structure of the complex of the catalase with the classical catalase inhibitor 3-amino-1,2,4-triazole (3TR) was determined at 1.95 Å resolution. Surprisingly, no binding to the heme site was observed; instead, 3TR occupies a binding site corresponding to the NADPH-binding pocket in mammalian catalases at the entrance to a lateral channel leading to the heme. Kinetic analysis of site-directed mutants supports the assignment of this pocket as the binding site for oxidase substrates

Critical Roles of the WASP N-Terminal Domain and Btk in LPS-Induced Inflammatory Response in Macrophages

While Wiskott-Aldrich syndrome protein (WASP) plays critical roles in TCR signaling as an adaptor molecule, how it transduces innate immune signals remains to be elucidated. To investigate the roles of WASP in innate immune cells, we established bone marrow-derived macrophage (BMDM) cell lines from WASP15 transgenic (Tg) mice overexpressing the WASP N-terminal region (exons 1–5). Upon LPS stimulation, WASP15 Tg BMDM cell lines produce lower levels of inflammatory cytokines, such as TNF-α, IL-6, and IL-12p40 than the wild-type BMDM cell line. In addition, the production of nitric oxide by WASP15 Tg BMDM cells in response to LPS and IFN-γ was significantly impaired. Furthermore, we uncovered that the WASP N-terminal domain associates with the Src homology (SH) 3 domain of Bruton's tyrosine kinase (Btk). Overexpression of the WASP N-terminal domain diminishes the extent of tyrosine phosphorylation of endogenous WASP in WASP15 Tg BMDM cells, possibly by interfering with the specific binding between endogenous WASP and Btk during LPS signaling. These observations strongly suggest that the interaction between WASP N-terminal domain and Btk plays important roles in the LPS signaling cascade in innate immunity

The data hungry home

It's said that the pleasure is in the giving, not the receiving. This belief is validated by how humans interact with their family, friends and society as well as their gardens, homes, and pets. Yet for ubiquitous devices, this dynamic is reversed with devices as the donors and owners as the recipients. This paper explores an alternative paradigm where these devices are elevated, becoming members of Data Hungry Homes, allowing us to build relationships with them using the principles that we apply to family, pets or houseplants. These devices are developed to fit into a new concept of the home, can symbiotically interact with us and possess needs and traits that yield unexpected positive or negative outcomes from interacting with them. Such relationships could enrich our lives through our endeavours to “feed” our Data Hungry Homes, possibly leading us to explore new avenues and interactions outside and inside the home

Metabolic Regulation of Invadopodia and Invasion by Acetyl-CoA Carboxylase 1 and De novo Lipogenesis

Invadopodia are membrane protrusions that facilitate matrix degradation and cellular invasion. Although lipids have been implicated in several aspects of invadopodia formation, the contributions of de novo fatty acid synthesis and lipogenesis have not been defined. Inhibition of acetyl-CoA carboxylase 1 (ACC1), the committed step of fatty acid synthesis, reduced invadopodia formation in Src-transformed 3T3 (3T3-Src) cells, and also decreased the ability to degrade gelatin. Inhibition of fatty acid synthesis through AMP-activated kinase (AMPK) activation and ACC phosphorylation also decreased invadopodia incidence. The addition of exogenous 16∶0 and 18∶1 fatty acid, products of de novo fatty acid synthesis, restored invadopodia and gelatin degradation to cells with decreased ACC1 activity. Pharmacological inhibition of ACC also altered the phospholipid profile of 3T3-Src cells, with the majority of changes occurring in the phosphatidylcholine (PC) species. Exogenous supplementation with the most abundant PC species, 34∶1 PC, restored invadopodia incidence, the ability to degrade gelatin and the ability to invade through matrigel to cells deficient in ACC1 activity. On the other hand, 30∶0 PC did not restore invadopodia and 36∶2 PC only restored invadopodia incidence and gelatin degradation, but not cellular invasion through matrigel. Pharmacological inhibition of ACC also reduced the ability of MDA-MB-231 breast, Snb19 glioblastoma, and PC-3 prostate cancer cells to invade through matrigel. Invasion of PC-3 cells through matrigel was also restored by 34∶1 PC supplementation. Collectively, the data elucidate the novel metabolic regulation of invadopodia and the invasive process by de novo fatty acid synthesis and lipogenesis

The Extra Domain A of Fibronectin Increases VEGF-C Expression in Colorectal Carcinoma Involving the PI3K/AKT Signaling Pathway

The extra domain A (EDA)-containing fibronectin (EDA-FN), an alternatively spliced form of the extracellular matrix protein fibronectin, is predominantly expressed in various malignancies but not in normal tissues. In the present study, we investigated the potential pro-lymphangiogenesis effects of extra domain A (EDA)-mediated vascular endothelial growth factor-C (VEGF-C) secretion in colorectal carcinoma (CRC). We detected the expressions of EDA and VEGF-C in 52 human colorectal tumor tissues and their surrounding mucosae by immunohistochemical analysis, and further tested the correlation between the expressions of these two proteins in aforementioned CRC tissues. Both EDA and VEGF-C were abundantly expressed in the specimens of human CRC tissues. And VEGF-C was associated with increased expression of EDA in human CRC according to linear regression analysis. Besides, EDA expression was significantly correlated with lymph node metastasis, tumor differentiation and clinical stage by clinicopathological analysis of tissue microarrays containing tumor tissues of 115 CRC patients. Then, human CRC cell SW480 was transfected with lentivectors to elicit expression of shRNA against EDA (shRNA-EDA), and SW620 was transfected with a lentiviral vector to overexpress EDA (pGC-FU-EDA), respectively. We confirmed that VEGF-C was upregulated in EDA-overexpressed cells, and downregulated in shRNA-EDA cells. Moreover, a PI3K-dependent signaling pathway was found to be involved in EDA-mediated VEGF-C secretion. The in vivo result demonstrated that EDA could promote tumor growth and tumor-induced lymphangiogenesis in mouse xenograft models. Our findings provide evidence that EDA could play a role in tumor-induced lymphangiogenesis via upregulating autocrine secretion of VEGF-C in colorectal cancer, which is associated with the PI3K/Akt-dependent pathway

Cytoskeletal control of B cell responses to antigens.

The actin cytoskeleton is essential for cell mechanics and has increasingly been implicated in the regulation of cell signalling. In B cells, the actin cytoskeleton is extensively coupled to B cell receptor (BCR) signalling pathways, and defects of the actin cytoskeleton can either promote or suppress B cell activation. Recent insights from studies using single-cell imaging and biophysical techniques suggest that actin orchestrates BCR signalling at the plasma membrane through effects on protein diffusion and that it regulates antigen discrimination through the biomechanics of immune synapses. These mechanical functions also have a role in the adaptation of B cell subsets to specialized tasks during antibody responses