Emborghart5242

Justicia procumbens is a food and medicine homologous variety, popularly used for making vegetable soups. In this study, a novel mesoporous silica was synthesized and used as the sorbent of SPE for the purification of lignans from J. procumbens. A laboratory-made SPE cartridge was packed with 100 mg of mesoporous silica, which was washed with 10% methanol and eluted using 0.8 mL acetonitrile after sample loading. Afterward, the extract was analyzed by ultra-performance liquid chromatography (UPLC) and MS/MS. All the lignans were efficiently separated in 6 min with the noise level in the range of 50-150 cps. 6'-Hydroxy justicidin B, 6'-hydroxy justicidin A, justicidin B, chinensinaphthol methyl ether, justicidin C, and neojusticdin A were identified to be the dominant molecular species in J. procumbens with contents of 0.065-0.37 mg/g in three tested sample batches from different geographic origins. In conclusion, the proposed mesoporous silica based SPE UPLC-MS/MS method is efficient in linearity (R2 = 0.9989-0.9996), sensitivity (LOD ≤0.13 μg/kg and LOQ ≤0.42 μg/kg), precision (RSDintra-day ≤3.12 and RSDinter-day ≤4.56), and recovery (83.42-96.11%, RSD ≤2.88%). © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.BACKGROUND There is a lack of evidence to assess whether gait functionality can be affected by the condition of the pelvic floor musculature in patients with multiple sclerosis (MS). OBJECTIVE To evaluate the relationship between pelvic floor functionality and general functional performance, and also their relationship depending on dependence degree in MS patients. PARTICIPANTS Forty-three MS patients performed the study. this website The pelvic floor musculature and its functionality were evaluated by urinary incontinence (UI), fecal incontinence, and constipation. General functional performance was evaluated by the Barthel index, the Health Status Questionnaire Short Form-12 (SF-12), and the Timed Up and Go (TUG) test. RESULTS UI was moderately related to general functional performance (SF-12 Physical R = -0.413; Barthel index R = -0.501; TUG R = 0.482). The comparative analysis showed differences between UI and gait functionality (P = .008), with poorer results in the TUG in patients with moderate/severe dependence (P  less then  .001). CONCLUSION UI appears to have a negative impact on the performance of daily living activities, walking, and the physical dimension of quality of life in patients with MS. In addition, patients with moderate or severe dependence showed higher UI and gait disturbance compared with those with mild dependence or independence. © 2020 Wiley Periodicals, Inc.In the original article Fig. link2 3 is not displayed correctly. The corrected figure follows.Glioblastoma (GBM) develops from adult brain white matter and is the most common and lethal primary brain tumor, characterized by rapid growth and invasion. GBM tumors frequently spread into the contralateral hemisphere, including in the beginning of tumor development. However, after complete resection of the tumor mass and chemo-radiotherapy, GBM commonly recurs around the tumor removal site, suggesting that the microenvironment at the tumor border provides therapeutic resistance to GBM cells. To improve patient prognosis, understanding the microenvironment at the tumor border is critical. Several microRNAs (miRNAs) show higher expression at the tumor border, with the top three involved in oligodendrocyte differentiation. Oligodendrocyte progenitor cells (OPCs) may induce stemness and chemo-radioresistance in GBM cells, providing a supportive function to promote GBM. This review describes important features of OPCs and insights into the "border niche," a unique microenvironment that allows GBM cells to survive and recur at the tumor border.Tumor lymphatics play a key role in cancer progression as they are solely responsible for transporting malignant cells to regional lymph nodes (LNs), a process that precedes and promotes systemic lethal spread. It is broadly accepted that tumor lymphatic sprouting is induced mainly by soluble factors derived from tumor-associated macrophages (TAMs) and malignant cells. However, emerging evidence strongly suggests that a subset of TAMs, myeloid-lymphatic endothelial cell progenitors (M-LECP), also contribute to the expansion of lymphatics through both secretion of paracrine factors and a self-autonomous mode. M-LECP are derived from bone marrow (BM) precursors of the monocyte-macrophage lineage and characterized by unique co-expression of markers identifying lymphatic endothelial cells (LEC), stem cells, M2-type macrophages, and myeloid-derived immunosuppressive cells. This review describes current evidence for the origin of M-LECP in the bone marrow, their recruitment tumors and intratumoral trafficking, similarities to other TAM subsets, and mechanisms promoting tumor lymphatics. We also describe M-LECP integration into preexisting lymphatic vessels and discuss potential mechanisms and significance of this event. We conclude that improved mechanistic understanding of M-LECP functions within the tumor environment may lead to new therapeutic approaches to suppress tumor lymphangiogenesis and metastasis to lymph nodes.Angiogenesis is a critical process required for tumor progression. Newly formed blood vessels provide nutrition and oxygen to the tumor contributing to its growth and development. However, endothelium also plays other functions that promote tumor metastasis. link3 It is involved in intravasation, which allows invasive cancer cells to translocate into the blood vessel lumen. This phenomenon is an important stage for cancer metastasis. Besides direct association with cancer development, endothelial cells are one of the main sources of cancer-associated fibroblasts (CAFs). The heterogeneous group of CAFs is the main inductor of migration and invasion abilities of cancer cells. Therefore, the endothelium is also indirectly responsible for metastasis. Considering the above, the endothelium is one of the important targets of anticancer therapy. In the chapter, we will present mechanisms regulating endothelial function, dependent on cancer and cancer niche cells. We will focus on possibilities of suppressing pro-metastatic endothelial functions, applied in anti-cancer therapies.Pancreatic cancer is one of the most challenging adenocarcinomas due to its hostile molecular behavior and complex tumor microenvironment. It has been recently postulated that pancreatic stellate cells (PSCs), the resident lipid-storing cells of the pancreas, are important components of the tumor microenvironment as they can transdifferentiate into highly proliferative myofibroblasts in the context of tissue injury. Targeting tumor-stromal crosstalk in the tumor microenvironment has emerged as a promising therapeutic strategy against pancreatic cancer progression and metastasis. This chapter brings a broad view on the biological and pathological role of PSCs in the pancreas, activated stellate cells in the onset of tissue fibrosis, and tumor progression with particular emphasis on the bidirectional interactions between tumor cells and PSCs. Further, potential therapeutic regimens targeting activated PSCs in the pre-clinical and clinical trials are discussed.Hepatocellular carcinoma and intrahepatic cholangiocarcinoma are the most common types of primary liver cancers. Moreover, the liver is the second most frequently involved organ in cancer metastasis after lymph nodes. The tumor microenvironment is crucial for the development of both primary and secondary liver cancers. The hepatic microenvironment consists of multiple cell types, including liver sinusoidal endothelial cells, Kupffer cells, natural killer cells, liver-associated lymphocytes, and hepatic stellate cells (HSCs). The microenvironment of a normal liver changes to a tumor microenvironment when tumor cells exist or tumor cells migrate to and multiply in the liver. Interactions between tumor cells and non-transformed cells generate a tumor microenvironment that contributes significantly to tumor progression. HSCs play a central role in the tumor microenvironment crosstalk. As this crosstalk is crucial for liver carcinogenesis and liver-tumor development, elucidating the mechanism underlying the interaction of HSCs with the tumor microenvironment could provide potential therapeutic targets for liver cancer.The interactions between tumor cells and the non-malignant stromal and immune cells that make up the tumor microenvironment (TME) are critical to the pathophysiology of cancer. Mesenchymal stem cells (MSCs) are multipotent stromal stem cells found within most cancers and play a critical role influencing the formation and function of the TME. MSCs have been reported to support tumor growth through a variety of mechanisms including (i) differentiation into other pro-tumorigenic stromal components, (ii) suppression of the immune response, (iii) promotion of angiogenesis, (iv) enhancement of an epithelial-mesenchymal transition (EMT), (v) enrichment of cancer stem-like cells (CSC), (vi) increase in tumor cell survival, and (vii) promotion of tumor metastasis. In contrast, MSCs have also been reported to have antitumorigenic functions including (i) enhancement of the immune response, (ii) inhibition of angiogenesis, (iii) regulation of cellular signaling, and (iv) induction of tumor cell apoptosis. Although literature supporting both arguments exists, most studies point to MSCs acting in a cancer supporting role within the confines of the TME. Tumor-suppressive effects are observed when MSCs are used in higher ratios to tumor cells. Additionally, MSC function appears to be tissue type dependent and may rely on cancer education to reprogram a naïve MSC with antitumor effects into a cancer-educated or cancer-associated MSC (CA-MSC) which develops pro-tumorigenic function. Further work is required to delineate the complex crosstalk between MSCs and other components of the TME to accurately assess the impact of MSCs on cancer initiation, growth, and spread.The implications of a tumor microenvironment in cancer initiation and progression have drawn interest in recent years. Within the tumor stroma, fibroblasts represent a predominant cell type and are responsible for the majority of extracellular components within the tumor microenvironment, such as matrix and soluble factors. A switch from quiescent fibroblasts to cancer-associated fibroblasts triggers a large variety of pro-tumorigenic signals that support tumor progression and shape the surrounding pathological stroma, with the remodeling of tissue architecture and repression of the local immune response. The heterogeneous nature of cancer-associated fibroblasts and their multiple functions are subject of active research as they could represent promising targets for cutting-edge therapeutic approaches to cancer and the tumor microenvironment.Adipose tissue contribution to body mass ranges from 6% in male athletes to over 25% in obese men and over 30% in obese women. Crosstalk between adipocytes and cancer cells that exist in close proximity can lead to changes in the function and phenotype of both cell types. These interactions actively alter the tumour microenvironment (TME). Obesity is one of the major risk factors for multiple types of cancer, including breast cancer. In obesity, the increase in both size and number of adipocytes leads to instability of the TME, as well as increased hypoxia within the TME, which further enhances tumour invasion and metastasis. In this chapter, we will discuss the diverse aspects of adipocytes and adipocyte-derived factors that affect the TME as well as tumour progression and metastasis. In addition, we discuss how obesity affects the TME. We focus primarily on breast cancer but discuss what is known in other cancer types when relevant. We finish by discussing the studies needed to further understand these complex interactions.